BIO 451 Final Exam Review Questions (Beginning of the semester through Microbial Symbionts.

New material
starts with “Intro to Infectious Disease”)

Questions shown in red can be skipped in your final exam studying.

Introduction

b. How do you know if a complex of molecules is alive or not?

c. What are the characteristics of the six major kingdoms of life?
d. What are the characteristics of the three major domains of life?
e. How can a small rRNA be used to construct the “tree of life?”
f. What are the major structural features of a prokaryotic cell?
g. What are the major structural features of a eukaryotic cell?
h. Which structures are common to both cell types?
i. Which structures are unique to one type or the other?
p. What is the process of diffusion?
q. How might the concentrations of molecules in a cell affect their rates of diffusion?
r. What is the distribution of molecules and organelles in a bacterial cell?
t. What is metabolism?
v. How do new molecules enter a metabolic pool? How do they leave it?

Microscopic Methods

a. Why is it necessary to use microscopes to study microorganisms?

c. Why are most lenses in a modern microscope compound lenses?
d. What factors limit the resolution of a light microscope?
e. How can the resolution be improved?
g. Why is it necessary to stain most microorganisms?
h. Which microbes can be seen without staining?
i. What is the difference between a positive stain and a negative stain?
j. What is meant by a differential stain?
k. What is different about the optics of a dark field microscope?
l. What is different about the optics of a phase contrast microscope?
m. What is the advantage of phase contrast microscopy over standard light microscopy of a stained
sample?
o. What the source of the fluorescence in this system?
p. How does an electron microscope work?
q. What is required in preparing a sample for transmission electron microscopy?
r. What is the resolution of an electron microscope?
s. What structures can you see with an electron microscope that you cannot see with
a light microscope?
t. What is the value of negative staining or shadow casting in electron microscopy?
v. What is the purpose of a scanning electron microscope?

Pure Cultures

1. Why is cultivation in the lab necessary for the characterization of microorganisms?

5. Why is agar used as a gelling agent for microbiological media and not some other agent like gelatin?
6. Describe the steps that comprise Koch’s postulate.
-Can the steps always be done? Should they be done with human pathogens?
8. What is a colony? How does it compare to a clone?
9. What types of variations occur in a microbial culture, either in a liquid culture or in a colony on an agar plate?
10. How can you explain these variations?
11. What is a mutation? How does the occurrence of spontaneous mutations change the phenotype of a culture?
12. What causes bacteria to die? Why might some cells in a culture be alive and others be dead?
13. What is the basis of staining them differently?
15. What is the purpose of streaking bacteria on an agar plate?
16. Why is it important to start a new culture with a single colony?
17. What are the key chemical elements in any microbiological medium? Why are they essential?
18. Compare a defined medium, an enriched medium, and a differential medium. Give an example of each and
explain when each might be used.
19. What are the key physical factors that can limit bacterial growth?

Molecular Techniques

a. What are the major macromolecules in a bacterial cell?

c. How does “omic” analysis differ from more traditional ways to characterize bacteria?
d. How does a bacterial plasmid differ from a bacterial chromosome?
e. How does a bacterial chromosome differ from a eukaryotic chromosome?
f. In what ways do mitochondrial and chloroplast DNAs resemble bacterial DNAs?
g. What is the value of DNA sequencing? Why have scientists put so much time and effort into developing
methods for rapidly sequencing large DNA molecules?
m. Why do transcriptomes vary with time or growth conditions?
n. Which RNAs comprise a transcriptome?
o. What is the basis of microarray analysis? How does it work? What can it tell you about a microorganism?
p. How does RNA-Seq analysis work? How is it different from whole-molecule sequencing?
r. Why do proteomes vary with time or growth conditions?
v. What is metabolism?
w. What compounds make up a metabolome?
x. How can similar compounds in a metabolome be separated and quantified?

Prokaryotic Cell Structure I, II, III, IV

I.
a. What are the general features of a prokaryotic cell? Which organelles also occur in eukaryotic cells? Which
organelles in eukaryotic cells do not occur in prokaryotic cells?
b. What types of shapes are seen among bacteria?
e. What components commonly comprise a bacterial cell envelope? Do all of them occur in every cell?
f. What is the Gram stain? What color do Gram-positive cells appear after staining? What color do Gram-
negative cells appear after staining? Why might some microorganisms be “Gram-variable” or give
inconsistent reactions in the staining procedure?
g. What is the basic structure of a Gram-positive cell wall?
h. What is the basic structure of a Gram-negative cell wall?
i. How do the walls of Deinococcus and Mycobacterium differ from these basic patterns?
j. What is unusual about the Mycoplasmas?
k. What sorts of cell walls are found among the archaea?
l. Why might these walls vary so much from one another?
m. Give the three basic functions of a cell wall. In addition to these functions, what other roles might a cell
wall play in the biology of a microorganism?
n. What is a peptidoglycan? Diagram a peptidoglycan as a series of chemical blocks (that is, draw it
schematically, not in terms of its detailed chemical structure).
o. What might be the evolutionary advantage to including D-amino acids in the structure of a peptidoglycan?
p. What variations in peptidoglycan structure commonly occur?
u. What is a periplasm? Why is the periplasm in a Gram-positive cell less well-defined than that in a Gram-
negative cell?
v. Where is the peptidoglycan found in a Gram-negative bacterium? How is it connected to the other
components of the cell envelope?
w. What is the structure of an outer membrane? How does it differ from a cell or plasma membrane?
x. What is the structure of a lipopolysaccharide? What is its function?
y. How do lipopolysaccharides vary? Why are they said to be antigens?
z. What is a porin complex? What is its function?

II.
a. Why are the terms cell membrane, plasma membrane, and phospholipid bilayer often used as if they were
synonymous?
d. Are the two leaflets of the plasma membrane bilayer the same?
e. How does the plasma membrane differ from the outer membrane in gram negative bacteria?
f. How do the lipids of the Archaea differ from those of the Bacteria?
h. What is meant by membrane fluidity? Why is it important?
l. What are the functions of the cell membrane?
m. Why is the protein to lipid ratio is a bacterial cell membrane so high?
p. How are the thylakoids and cristae of chloroplasts and mitochondria similar to these
membrane invaginations?
r. What is the function of an anammoxosome?
u. What is a nucleoid? How does it differ from a nucleus? How does it differ from a plasmid?
v. What types of proteins are associated with the nucleoid? What are their functions?
x. What is the structure of a bacterial ribosome?
y. What is the evidence that transcription and translation are coupled in bacteria?
z. What are the advantages to coupling transcription and translation?

IV.
a. What is an S layer? Where does it occur in a Gram-positive bacterium or in a Gram-negative bacterium?
b. How does a capsule differ from an S layer?
e. What is the composition of a capsule?
f. Why might some capsules be more rigid and others much looser?
g. What is the function of a capsule?
h. What is a biofilm? How is it formed? How does it grow?
m. What is the role of the sex pilus in conjugation?
n. What other functions do pili have?
o. How does a flagellum differ from a pilus?
r. How does a flagellum achieve cellular movement?
w. What is meant by gliding motility?
x. How is a cell propelled in the case of gliding motility?

Eukaryotic Cell Structure

a. Which of the structures found in a prokaryotic microorganism are also found in a eukaryotic
microorganism?
b. Which structures are unique to eukaryotic microorganisms?
c. What happens during the process of phagocytosis? How does phagocytosis contribute to
food acquisition? What are some of the other functions of phagocytosis?
f. What is the function of the nucleolus? How are new ribosomes made and exported to
the cytoplasm?
j. What are differences between the two major pathways for protein synthesis and localization?
k. Why is it necessary to import some proteins into mitochondria and chloroplasts?
l. What are the components of the endomembrane system?
m. Why is the potential for membrane budding and fusion so critical to the operation of this system?
n. What are the morphological and functional differences between rough
endoplasmic reticulum and smooth endoplasmic reticulum?
o. What is the structure and function of a lysosome?
p. How are lysosomes formed?
q. How do materials get into lysosomes prior to degradation?

Viruses and Other Acellular Entities

a. How does a virus differ from a living prokaryotic or eukaryotic cell?

b. Where does a virus get its energy? Where does it get its nucleotides for DNA or RNA
synthesis? Where does it get its amino acids for protein synthesis?
d Differentiate between naked and enveloped viruses.
g. What is the relationship between size and genome complexity?
h. Why are most plant viruses naked?
i. How are viruses classified?
j. Why does the book say that virus taxonomy is artificial?
k. Why might the human immunodeficiency virus (HIV) and the simian
immunodeficiency virus (SIV) show some similarities?
o. What are the major types of viral polymerases?
-Which might be provided by a host cell?
-Which must be encoded by viral genes?
p. What are the major portals of entry into a human host for a virus?
q. How do viruses attach to host cells? Which molecules act as receptors?
r. Why do viruses have a harder time getting into plant cells?
s. What are the three major mechanisms of viral entry into an animal host cell?
t. In which cases is the envelope retained or lost?
u. Why must a virus be “uncoated?’
v. Give some examples of proteins that might be made by early transcription and
translation.
w. Give some examples of proteins that might be made by late transcription and
translation.
x. Why might many viral proteins be made as polyproteins?
y. What is involved in virus assembly?
z. How are viruses released from host cells?
aa. Does virus reproduction always lead to host cell death?
bb. Describe the process by which a (+) strand RNA virus like the polio virus is reproduced.
cc. Why might some steps occur with a host membrane vesicle?
dd. What is the function of a RNA replicase?
ee. Describe the process by which a (-) strand RNA virus like the influenza virus is
reproduced.
ff. What are the advantages and disadvantages to having a segmented genome?
gg. What are the implications of a segmented genome on the development of a vaccine against
the flu?
hh. Describe the process by which a (+) strand retrovirus like HIV is reproduced.
-Which steps occur in the cytoplasm? Which occur in the nucleus?
ii. What is the advantage to forming a DNA intermediate that can be integrated into a
chromosome?
jj. Describe the process by which a double stranded DNA virus like the herpes virus is
reproduced.
-Which steps occur in the cytoplasm? Which occur in the nucleus?
kk. How does lytic reproduction of a bacterial virus differ from lysogenic
reproduction?
mm. What are the different types of viral infections in a human?
nn. Give an example of a virus that causes an acute infection.
oo. Give an example of a virus that causes latent infection.
pp. How does Herpes virus latent? How does Varicella-Zoster virus become latent?
qq. How does a viroid differ from a virus?
rr. How can a viroid cause a disease if it does not code for anything?
tt. How does a prion differ from a virus?
uu. How can a prion cause a disease if it does not code for anything?
vv. What is the function of a normal PrP protein? Where does it occur?
ww. How are prions transmitted?

Microbial Metabolism

a. What are the two major functions of metabolism?

b. Distinguish between a phototroph and a chemotroph.
c. Distinguish between an autotroph and a heterotroph.
d. Give an example of an organism that is a chemoheterotroph and an example of an organism that
is a photoautotroph.
e. Differentiate between anabolism and catabolism. How are anabolic processes
connected to catabolic processes?
f. What is a metabolic pathway? Why does a metabolic pathway normally involve multiple steps?
Why is a different enzyme needed for each step?
h. What is the difference between aerobic metabolism and anaerobic metabolism? What types of
processes occur under each condition?
i. What are the major forms of cellular energy? How can energy be converted from one form to
another?
j. Why are ionic gradients formed and maintained by cells?
m. What is the difference between an oxidation reaction and a reduction reaction?
n. What are the major electron carriers in cells?
o. How do possible nutrients pass through the envelope of a Gram-positive bacterium?
How do they pass through the envelope of a Gram-negative bacterium?
p. Differentiate between the four major modes of protein-mediated transport. What is the energy
source in each case? How is the specificity of each type of transport determined?
q. What happens during glycolysis? How is energy captured in a usable form?
r. What is a fermentation? How does a fermentation differ from a respiration?
s. How is ATP formed during a fermentation?
t. How is NADH formed during glycolysis converted back to NAD+ in fermentation?
u. What types of organisms carry out alcoholic fermentation? What types carry out lactic acid
fermentation?
v. How does electron transport lead to ATP formation?
w. Why is more ATP formed during aerobic respiration than during most
fermentations?
x. How do bacteria vary in the organization of their electron transport chains?
Why is this variation important?
y. How does anaerobic respiration differ from aerobic respiration?
aa. What is the role of anaerobic respiration in the global nitrogen cycle?
bb. What is the role of anaerobic respiration in the global sulfur cycle?
cc. What is a chemolithotroph? What types of substrates are used by these organisms as energy
sources? What are the products?
dd. Most chemolithotrophs are also autotrophs. What is required for autotrophic
metabolism?
ee. What is a phototroph? What is the role of light in their metabolism?

Microbial Growth

a. What is meant by binary fission?

c. What is the generation time of a single cell? Why is this usually not a fixed quantity?
d. Why is bacterial growth said to be exponential?
f. Why do different organisms have different generation times?
g. What is meant by a cell cycle?
h. What are the stages of the cell cycle in eukaryotes? What are the corresponding stages in
prokaryotes?
i. Why is it necessary to study the cell cycle in synchronized cultures of bacteria?
j. How can a synchronized culture be established? Why does synchrony slowly fall apart?
k. What happens during DNA synthesis?
l. What are the G1, C, and D periods? How do they vary in different cell cycles?
m. Why do replication cycles overlap in different cell cycles?
n. How does a batch culture differ from a continuous culture?
o. What are the stages of the cultural cycle of a batch culture?What happens during each of the stages?
p. How is the progress of a batch culture followed experimentally?
q. Why is death normally an exponential process?
r. How is a continuous culture set up?
s. What determines the growth rate in a continuous culture?
t. What are the effects of increased temperature on microbial growth?
w. What are the factors that allow a microorganism to grow at high temperatures?
x. What are the effects of pH on microbial growth?
z. How do bacteria attempt to maintain a constant internal pH even as the external pH
changes?
aa. What are the effects of external solutes on microbial growth?
bb. What is meant by a reactive oxygen species (ROS)? What are some examples?
cc. Why are reactive oxygen species toxic to a cell? What is an example of an enzyme involved in the
metabolism of ROS?
dd. Why are so many bacteria found in aerobic habitats pigmented?

Prokaryotic Gene Regulation

c. What is the different between a plasmid and a circular chromosome?

d. Why is it an evolutionary advantage to have some genes in a microorganism on a
plasmid?
e. How does gene density vary among different organisms?
h. What are the major features of a transcription unit? Why are many bacterial
transcription units said to be polycistronic?
i. Describe the process of transcription.
k. Describe the two major mechanisms of transcription termination.
l. Differentiate between a positive control system and a negative control system.
m. Differentiate between an inducible system and a repressible system.Give examples of each.
n. How do the regulatory proteins that control transcription recognize particular DNA
sequences?
o. Describe how the lac operon works
p. What is the difference between an operon, regulon, and modulon?
q. How are mRNA degraded?
r. What features influence the rate of mRNA degradation?
s. How does mRNA secondary structure control translation?
t. By what other mechanisms can translation be controlled?

Prokaryotic Genomes
a. What are the differences between an organism’s genotype and its phenotype?
b. For a bacterium, what are some common examples of phenotypes?
c. How would you show that a bacterium was ampicillin sensitive or ampicillin
resistant?
 d. How would you show that a bacterium is a histidine auxotroph or a prototroph?
e. What is the difference between sexual and asexual reproduction?
f. What are the differences among the three major parasexual processes?
g. What are the essential features of transformation?
h. How does transformation on a Gram-positive bacterium differ from
transformation in a Gram-negative bacterium?
i. What are the general properties of a plasmid?
j. How does a conjugative plasmid differ from a non-conjugative plasmid?
k. How is F replicated and transmitted during normal cell division?
l. What happens during mating between an F+ cell and a F- cell?
m. Describe the process of rolling circle replication.
n. How does transduction differ from conjugation?
o. How is a generalized transducing particle formed?
p. How much of the genome does this particle carry?
q. How does specialized transduction differ from generalizing transduction?What happens when the
DNA in this particle is introduced into a recipient?

Microbial Ecosystems

1. What is a microbial ecosystem? Give 3 examples of microbial ecosystems in specific areas of earth
2. Approximately what percentage of microbes are culturable? Why do you think it is so low?
3. What is a niche? What changes in microenvironments allow for different microbial niches?
4. Explain how biofilms are formed, where they are found in nature, and how they contribute to human
infections. Give examples of human infections caused by biofilms
5. Discuss approximate values of prokaryotic biomass and productivity in different environments.
6. How do we define a bacterial species and how is it fundamentally different from defining a eukaryotic species?
7. Why are most oceanic prokaryotes oligotrophs? How does eutrophication lead to dead zones?
8. Describe the pattern of microbial distribution in the different oceanic zones.
10. What is the approximate ratio of viruses: prokaryotes in the ocean? How could this potentially affect gene
transfer among organisms and other species interactions and microbial evolution?
11. How are microbes in freshwater ecosystems different from saltwater microbes?
13. What is the rhizosphere and what specific factors enable high support of microbes in this region?
14. Describe the different types of microbes that exist in the rhizosphere and explain how this is different from the
microbial content of soil outside the rhizosphere.
15. What are xenobiotics and why are they a problem in the environment?
16. Describe the process of bioremediation. What are examples of electron donors and acceptors that are either
contaminants or are a form of biostimulation?
17. What is MNA, biostimulation, and bioaugmentation?
18. Describe and draw a deepsea thermal vent and associated microbes. Where do these vents occur, why do
thermal vents exist, and how do they support microbes?

Microbiology of Food and Water

1. What are the extrinsic and intrinsic factors that affect microbial growth in foods?
2. What is water activity, and how does it affect microbial growth? Give examples of foods with varying levels of
water activity.
3. Why is fungal spoilage more common on fruits than vegetables?
7. We discussed 6 ways to reduce food spoilage. List and describe each of them and give examples of each
method.
8. What is botulism and why is it associated with improper canning of food?
10. Describe the process of yogurt production. What types of bacteria are used? Give example species and their
growth requirements and metabolic products.

11. What are starter cultures and why are they essential for commercial food production?
12. What types of traits are often found on mobile elements in starter culture bacteria and what have scientists
done to stabilize the presence of these characteristics in the bacteria?
14. What is the difference between a common source and a propagated epidemic?
15. What are the most common foodborne bacterial and viral infections in the United States?
16. What is the difference between foodborne intoxication and a foodborne illness? How would you treat each of
them?
17. Describe sources of drinking water and how each of these sources can become contaminated.
18. Taking into account the VICE News Global Water Crisis video we watched, why is fresh water shortage
predicted to be a global issue in the near future? What human activities have contributed to this, and what can be
done to improve the situation?
19. What do wastewater treatment plants do to water (be specific)?
20. How is drinking water purified?
21. What is the difference between fecal coliforms and coliforms and how are they used as indicator organisms?

Microbial Symbionts

1. What is a symbiont? What are the three different types of symbionts?

2. What is the difference between an ecto and an endosymbiont? What types of host organisms have
endosymbionts, and which ones don’t?
3. What are endophytes? What are rhizobia?
4. What benefits to plants provide to endophytes and what benefits do the endophytes provide to the plant?
5. What is leghemoglobin and why is it important to endophytes?
6. How is a root nodule formed?
7. Describe the metabolic processes that occur in root nodules. What types of carbon compounds are provided to
the bacteria from the plant?
10. How does microbial diversity differ among different surfaces of the body? What groups of bacteria are more
common in some areas compared to others?
11. What factors contribute to variation in the skin microbiome?
12. How do skin microbes contribute to the overall health of the host?
13. What are the unique aspects of the vagina that contribute to the types of microbes found there?
15. Describe how plaques form on the teeth.
16. How do the pH changes in the GI tract affect the diversity of gut microbes?
17. What metabolic activities do they perform?
18. What benefits do gut microbes provide to humans?
19. Why do you think fecal microbial transplantation has a higher likelihood of treatment success compared to the
use of probiotics? Give specific reasons.
20. Describe the process of FMT and hypothesize why it is effective for the treatment of C. diff infections when
antibiotics usually fail.

21. Hypothesize how obesity could be associated with specific gut microbial populations. Be specific in your
explanation.
22. How are colonic, cecal, and rumen fermenters different in their gut organization? Give an example organism
for each type.
23. What is coprophagia and what types of organisms exhibit this?
24. Describe rumen fermentation processes. What types of microbes are often involved, and what metabolic
processes do each do? Where do carbon-based and nitrogen-based compounds come from in the ruminant
animal’s diet?
25. What is the difference between primary and secondary endosymbionts in invertebrates?
26. Describe the microbial processes in the hindgut of the termite. How is the termite gut different from or similar
to the cow gut?

Chapter 17: Introduction to Infectious Diseases

1. Compare and contrast a disease, an infectious disease, and a zoonotic disease

Disease- is a disturbance in the normal functioning of an organism
Infectious diseases- are cause by microbes that can be transmitted from host to host
Zoonotic diseases- can be transmitted from animals to humans

2. What is a pathogen? What is pathogenesis?

A pathogen is a microbe that is associated with the production of disease. Pathogenesis – the process by
which pathogens cause disease.

3. What is the difference between primary and opportunistic pathogens? Give an example of each
Primary pathogens are ones that are able to cause disease within a multitude of uncompromised hosts. -
Opportunistic pathogens (include commensal organisms or environmental organisms) are ones that require
some sort of cut or someone to have a poor immune system to enter the body- the host must be compromised – C.
Diff.

4. What is meant by a pathogen’s virulence? What is the case-to-infection ratio? What is the case fatality rate?
A pathogen’s virulence is a measure of the severity of the disease the pathogen causes.
Case-to-infection ratio is the number of people who have been exposed to the pathogen – that have the
infection and that become diseased.
Case fatality rate is the number of people who have died from the disease.

5. What is a carrier host?

An organism that may be asymptomatic but spread the infectious agent.

6. What are the five steps a pathogen must do to cause disease (e.g. microbial virulence strategies)? Describe and
give examples of each.
Attachment/Invasion- protein:protein interactions
Replication
evade host defenses- antigenic variation, latency, capsules, replication within phagocytes, biofilm formation
exit-

7. Related to #6, describe specific host evasion strategies that pathogens can use.
Antigenic variation- shifting their surface protein structures- makes them hard to recognize
Capsules- makes hard for pathogen to be recognized
Biofilm formation- acts as a physical barrier
Entry into a phagocyte- replicates inside phagocyte and bursts
Latency- virus is dormant- not actively replicating, but still present within host genome.

8. Discuss the 5 routes of pathogen transmission that were listed in class. Give an example pathogen that is
transmitted by each of the routes.
Contact
Direct & Indirect
Fecal-oral
Respiratory (“aerosol”)
 Vector-borne
Sexual transmission

9. What is the difference between horizontal and vertical transmission of a pathogen? Give an example of both
transmission routes.
Horizontal – human:human
Transmission of a pathogen to another member of the same species other than a parent to offspring
Vertical- mother:baby
Passing of a pathogen from parent to child - HIV

10. Give an example of a zoonotic pathogen.

Rabies, Ebola (bats)

11. What is epidemiology?

The study of patterns of disease in populations

12. What is the difference between morbidity and mortality?

Morbidity rate- rate of disease in a population
Mortality rate- death rate of disease

13. What is the difference in jurisdiction of the CDC and the WHO?
CDC jurisdiction is within the US – WHO is global

14. What is the difference between incidence and prevalence?

Incidence – more specific- the number of new cases appearing in a population within a specific time period
Prevalence- the number of new cases appearing in a population at a particular time

15. Describe the differences among the following: endemic disease, epidemic disease, pandemic disease, and
outbreak.
Endemic disease- habitually present in the population
Incident rate increases are more susceptibles join the population
Incident rate decreases as there are more outbreaks that lead to more immune people.
Epidemic disease- incidence of a disease rises significantly above the normal expected value
Pandemic disease- a global epidemic- happening at a larger spread
Outbreak- unexpected cluster of cases in short time in a localized population

16. Describe the difference between a common source epidemic and a propagated epidemic.
Common source is when people receive the pathogen from the same thing- like a dirty drinking fountain.
A single source of infection to which the population is exposed
Propagated is when it is passed from human to human- everyone becomes a source
Infection that is passed from one host to another

17. List and describe Koch’s postulates. What are the molecular rules of Koch’s postulates?
Can be used to show that a specific microbe caused a specific disease.
- The suspected microbe is identified in every person with the disease, but not those without the illness
- A pure culture of the suspected microbe is obtained
- Experimental inoculation of the suspected microbe into a healthy test host causes the same illness
- The suspected microbe is recovered from the experimentally inoculated host organism.

18. What are some of the driving forces for pathogen evolution? Give examples of pathogens for each of the
driving forces described.
Encountering a new population
SIV  HIV
 Pathogens become more virulent
Pathogenic E. coli. Normally we have E. coli in our intestines, but horizontal gene transfer results in
the acquiring of virulence factor genes.
Methicillin-resistant S. aureus. Selective pressures of antibiotic overuse has led to the acquisition of
resistance traits against the drugs.

19. Why have polio levels significantly decreased over the past 60 years? What factors contribute to its persistence
in some areas of the world?
Polio levels have decreased because the vaccination has been very effective.

Chapter 18: Innate Immune System Review Questions

1. Describe the specific differences between the innate immune system and the adaptive immune system.
Innate immune system- the first line of defense. This system takes longer to get rid of a pathogen compared to
adaptive immune system. The molecules of the innate immune system include: Toll like receptors (TLRs), MBL
(Mannose-binding lectin), CRPs (C-reactive proteins), Complement proteins, and Interferons. These are all PRRs
(pattern recognition receptors) that recognize the PAMPs (pattern associated membrane protein) on the antigen
and bind to them for antigen destruction. The key to the innate immune system is phagocytosis.

MBLs and CRPs are opsonizing-secreted PRRs. The MBLs coat the mannose (PAMP) covered surface of an
antigen and tag them for opsonization. Opsonization is when a mannose covered yeast or bacteria is brought to a
macrophage/phagocyte by the tagging of MBL and is phagocytosed. The CRPs recognize the phospholipids of
bacteria and plasma membrane of fungi and tag the cell for opsonization.

In the lectin pathway, MBLs recognize mannose coated surfaces and the complement pathway is activated
which leads to opsonization. In the alternative pathway, complement proteins become activated in the presence of
PAMPs like lipoteichoic acid and lipopolysaccharides. This activates a cascade- which is when complement proteins
are released and bind together on the antigen to create a membrane-attack complex (MAC) which creates a pore in
the membrane of the antigen  inrushing fluid into the cell  lysis of the cell. This is the alternative pathway of
complement. The classical pathway of complement includes antibodies that recognize the antigen and activates the
complement pathway. This results in inflammation.

The adaptive immune system is comprised of T-cells and B-cells. This system is more efficient, in that it results in a
quicker response to antigens due to memory cells. BCRs and TCRs are created from gene rearrangement which
results in unique receptors. These are created before the exposure to pathogens. These memory cells are produced
from T cells and cytokine stimulation. The adaptive immune system deals with more issues within the cell rather than
outside the cell. The antigen is usually brought into the cell through phagocytosis or cell mediated endocytosis (if
antigen is exogenous). There, depending if it is an exogenous or endogenous antigen will be tagged with its
appropriate MHC (I/II). If it is exogenous, then the antigen binding cell will have the antigen peptide displayed on a
MHC II. The T cell will have a CD4 co-receptor along with its receptor. If it is an endogenous antigen, the T-cell will
have a CD8 co-receptor that will recognize MHC I on the antigen presenting complex (APC).

Naïve T-cells will receive the antigen (either exogenous or endogenous) and from there will undergo maturation
depending on the type of antigen. This will result in an effector cell and memory cell. The effector cell then releases
cytokines which indirectly help activate CD8 – cytotoxic cell activity. That cytotoxic t cell will need to bind to the
antigen and receive cytokine hormones from the T helper cell to create its own effector and memory cells. That
effector cell created will release granzymes and perforin that actively degrade the antigen. The memory cell will bind
to the antigen that is on the APC. That APC has the antigen peptide presented on a MHCI cell.

2. Describe the aspects of the skin that make it part of the innate immune system.
The skin is a physical barrier to pathogens. It also has low pH – an acidity around 5.0, it is cool, dry, dead skin
cells provide armor, antimicrobial oil (sebum) lies on top of this dead skin cell layer, sweat secretions also provide an
antimicrobial layer, and normal flora microbes that normally colonizes the skin can crowd out or starve out any
potential invaders.

3. Describe how the mucosal membranes form a barrier in the innate immune system
The mucosal membranes are interior surfaces that are coated with wet mucus. The mucus is moved along the
surface to prevent microbe attachment and the mucus contains antimicrobial molecules like defensing proteins,
lysozymes, lactoferrin. And there is competitive exclusion by flora again.

4. Describe the specific chemical innate defenses associated with mucosal membranes.
^

5. What proteins bind to iron in vertebrates? Why is it important to consider iron when understanding innate
immune defense and microbial invasion?
Depriving antigens of iron stops them from growing. Iron is a limiting element, and our bodies work to keep iron for
OUR cells. Some iron binding proteins include- hemoglobin, myoglobin, transferrin, lactoferrin, and ferritin.

6. What are the steps involved in inflammation and what are the consequences or general results that occur
following these steps? I.E. why is inflammation useful?
If there is a cut, the pathogen enters the body which then leads to the release of vasodilator molecules (like
histamine, prostaglandins, and serotonin), the bacteria multiply and invade tissue and concentrations of vasodilators
increase. The vessel dilates which allows more blood to the area. An increase in local temperature and redness
occurs. Vessel walls become more permeable (1st consequence of local inflammation – vasodilation) (& technically 3rd
consequence) . Fluid moves into the tissue, causing swelling. Extravasation (2nd consequence) of cells and molecules
occurs. Extravasation is the movement of cells and molecules into the interstitial space. Antibody and complement
factors bind to the bacteria. Phagocytes engulf and destroy the bacteria. Cytokines are released, attracting more
leukocytes. Adhesion molecules are expressed on vessel walls to facilitate extravasation of immune cells. Clotting is
initiated to restrict accoss of bacteria to circulatory system.
Consequences:
1. Vasodilation
2. Extravasation
3. Increased permeability in vessels

7. What is the difference between septic shock and toxic shock?

Septic shock is from widespread presence of bacteria in the body that induces system wide inflammation.
Toxic shock is from overstimulation of the immune response by bacterial exotoxins in the blood. (TSS- when you
leave a tampon in too long YAY PERIODS)

8. What are PAMPs? What are PRRs? How do they interact?

PAMPs- pathogen associated molecular patterns that are recognized by PRRs (pattern recognition receptors)
PAMPs are found on foreign microbes and not self-cells. PRRs are evolutionarily ancient and are found on
invertebrates, vertebrates and in plants. They recognize PAMPs and activate the response against them.

9. Why are some PRRs on the plasma membrane and others are on the cytoplasm or endosomal compartments?
Some PRRs are on the plasma membrane and in endosomal compartments because they can be found on any
nucleated cell. Bacterial components are commonly found on the plasma membrane so PRRs are required to trigger
internal signaling reactions if they find PAMP ligands.

10. What are Mannose-binding lectin and C-reactive protein and why are they considered PRRs?
These are opsonization secreted PRRs because they recognize PAMPs on antigens and opsonize them.
MBL recognizes mannose that is commonly found coating bacterial and yeast cells. CRP often recognizes
phospholipids on bacterial cells and the plasma membrane on fungal cells.

11. What is opsinization?

Opsinization is when a microbe is coated by the PRR which then enhances the destruction or uptake by other cells
like macrophages or phagocytes.

12. What is complement?

Complement are proteins that become activated in the presence of PAMPs and the activation leads to opsonization,
inflammation, and MAC formation.

13. What do type I interferons do? What specific impacts do they have on the host cell?
Type 1 interferons are cytokines that are secreted when viruses are detected. They have interferon alpha and beta.
These initiate an antiviral state. It cannot help already infected cells. For the good of the rest of the organism,
interferons kill the infected cell to stop the spread. These can also increase activities of antiviral cells like natural
killer cells. Interferons shut down viral activity through apoptosis  programmed cell death.

14. What are examples of phagocytes? Describe the process of phagocytosis.

Phagocytes can be macrophages, monocytes and neutrophils. They are immune system cells that engulf foreign
invaders. Usually opsonization can enhance uptake by the phagocyte. Once the invader is ingested, the vesicle
containing the microbe (phagosome) fuses with a lysosome to form a phagolysosome and the oxidative bursts and
lysosomal enzymes kill the microbe and exocytosis expels the debris.

15. What are the functions of eosinophils, basophils, and mast cells
These are basically natural killer cells but for bigger things. These cells help fight pathogens by releasing toxic
granule contents near them.

16. What are natural killer cells and how do they function?
Natural killer cells go around trying to recognize self or foreign cells. If they don’t recognize a cell as self, they
eliminate the host cell that is infected with the pathogen. They are not phagocytic. After contact is initiated, granule
components are released like perforin and granzymes. They look to recognize self-cells through the MHC I. With
perforin, a pore like complex is formed on the cell plasma membrane and with granzymes, they induce apoptosis.

Chapter 19: Adaptive Immune System

1. What is the difference between primary and secondary lymphoid tissue?

Primary lymphoid tissues are developed within the bone marrow. BCRs and TCRs are created through gene
rearrangements that make them very unique. Secondary lymphoid tissue is when these receptors mature and are
expelled into the peripheral blood.

2. What is the difference between primary and a secondary immune response in the adaptive immune system?
Primary response takes a lot longer than secondary immune response. Exposure to a new infectious agent produces
a primary immune response. This can take 7-14 days to peak, producing memory lymphocytes as a result and clearing
the pathogen. Subsequent exposure results in a memory response (secondary immune response). This response is
faster and more potent than the primary.
Primary initial response- chance that the pathogen was recognized by the receptors. The B and T cells mature
(maturation) (secondary immune response) to perfect binding to receptor and creates memory for the pathogen.

3. Describe the functions of T cells, how they are activated, etc

T cells are activated through
Antigen presentation
Cell signaling- lots of cytokines
Production of stimulatory molecules

4. Describe how a T cell can go from naïve to effector or memory cell.

Activated T cells expand and differentiate into either effector or memory cells.
5. How do TCRs and MHCs interact?
T-cell activation requires binding of the TCR with the specific peptide presented on major histocompatibility (MHC)
molecules of APCs (antigen presenting complexes). Co-receptors (either CD4 or CD8) must also correctly interact
with the MHC molecule
- CD4 interacts with MHC II
- CD8 interacts with MHC I

6. Describe the difference between memory cells and effector lymphocytes

Memory cells differentiate during initial adaptive immune responses.
Long lived
Produce a faster and more vigorous response when the same antigen is encountered again.
The speed of the 2nd (3rd or 4th) response can even prevent a repeat infection from occurring.
Effector cells are actions cells
Short lived
Armed with direct immune functions
In T cells, effector form depends on the co-receptors.
CD4+ t-cells = secretion of large amounts of cytokine to enhance (help) and direct actions of other immune
cells.
CD8+ t-cells= cytotoxic killing of infected cells by release of granzymes/perforin near contacted target cell,
initiating apoptosis. – similar to NK cells. They recognize intracellular problems

7. Describe the difference between how the adaptive immune system responds to exogenous antigens and how it
responds to endogenous antigens (cells involved, cell interactions, antigen processing, etc.)
Extracellular antigens are taken in by endocytosis
- Phagocytosis: takes in large objects (whole bacteria)
- Receptor-mediated endocytosis: initiated by binding of particles to cell-surface receptor molecules
Broken down and presented on MHC class II molecules
Restricts presentation to CD4+ T cells that can bind to MHC class II structures
Once presented, initiates activation of helper T cells
- Effectors (large amounts of cytokines)
- Memory (for later responses)
--
1) the cell takes up foreign molecules through receptor-mediated endocytosis and phagocytosis
2) the phagosome or endocytic vesicle forms
3) the vesicle fuses with a lysosome
4) digestion produces peptide fragments
5) the digestive vesicle fuses with a vesicle containing MHC II molecules
6) the MHC II molecules bind the peptides
7) the vesicle fuses with the plasma membrane transporting the MHC II peptide complexes to the cell surface.

1) Antigen presentation and binding by CD4+ t cell occurs

2) The activated CD4+ T cell secretes cytokines and expresses its receptor for autostimulation
3) Clonal expansion and differentiation produces a population of memory and effecter TH cells.

--
Intracellular antigens and the endogenous pathway
- Proteasomes fragment intracellular antigens
small peptide fragments loaded into MHC class I molecules
- Presentation restricted to CD8+ cytotoxic T cells that can bind to MHC class I structures
--
1) Proteins in the cytoplasm enter the proteasome and are degraded
2) The resulting peptides are transported to the endoplasmic reticulum
3) The peptides are loaded onto MHC I molecules
4) The MHC I:peptide complexes are transported to the Golgi apparatus
5) Membrane fusion of vesicles form the Golgi apparatus places MHC I: peptide complex on cell surface.

--
Activation of CD8+ T cells produces effector (killer) and memory cells.
The killer cells recognize targets by their presentation of antigen epitope fragments on MHC class I
Killing is achieved by T cell release of perforin/granzymes including apoptosis in target.

8. What are proteasomes and how are they important in endogenous antigen processing?
Proteasomes take in proteins and a ubiquitin and degrades the protein into peptides. These peptides then
enter the ER and are attached to MHC I molecules and are then transported to the Golgi apparatus. The Golgi
apparatus has membrane fusion of vesicles containing the MHC I:peptide complex that then get presented on the
cell surface.

9. Describe the steps involved in how a cytotoxic T cell can kill a cell
The cytotoxic T cell gets activated through the detection and binding to a MHC I: peptide complex. This
activates the release of granzymes and perforin that degrade the infected cell and causes apoptosis. The cell
fragments and microbes are then degraded by phagocytes.

10. What is a professional antigen-presenting cell?

A professional antigen presenting cell is one that present using MHC II. These are like dendritic cells,
macrophages, B cells, and they are highly active in taking in exogenous antigens and presenting them to helper T
cells.

11. Draw the pathway by which helper T cells can stimulate both the cell mediated and humoral immune response.
Label all antigens and cell receptors

12. Describe how antibodies are produced

 Antibodies are produced through the humoral response. A naïve B cell uptakes an antigen and then presents
that antigen peptide on MHC II for the CD4+ T helper cell to recognize. That T helper cell then releases cytokines that
activate that B cell to differentiate into an effector and memory cell. That effector cell is a plasma cell which creates
antibodies.

13. Describe the specific functions of antibodies

Plasma cells can quickly undergo apoptosis in around 2 days, but the antibodies that they secrete may last
for weeks in the blood. Plasma cells have fast production but they are short lived.
Antibody functions:
Blocks binding of pathogens/toxins on host cells
Fixes complement to bacterial structures, leading to lysis  classical pathway
Opsonization (increases phagocytosis)
Agglutination (clumping of antigen, increasing phagocytosis)
An FcR on a macrophage of a neutrophil recognizes and binds to Fc on the antibody and phagocytoses it.

Chapter 20: Bacterial Pathogenesis

1.) What is the difference between pathogenesis and disease?
Pathogenesis= process used by pathogens to produce disease
2.) What are the general mechanisms that both bacterial and viral pathogens have to survive and
reproduce in hosts?
a. Attach to our surfaces and tissues – attachment factors
b. Damage tissues to obtain nutrients and replicate
c. Avoid host immune responses
3.) What are virulence factors?
a. Pathogen products that enhance their ability to cause disease
4.) How do attachment factors work as virulence factors? What are two examples?
a. Fibronectin-binding proteins
i. Fibronectin= large plasma glycoprotein in plasma and extracelluar matrix
ii. Since it is everywhere in the body, it’s a prime target for pathogen binding
b. Fimbrae
i. Specilized pili with an adhesibe tip
1. Binds to different types of receptors
2. Acts as a “probe” to get beyond the repulsing negative charge on the host cell.
c. Various membrane associated molecules (capsules)

5.) What is the difference between endotoxins and exotoxins?

a. Endotoxins are a part of the cell wall structure and induce inflammatory responses
i. LPS on gram negative cells
ii. LTA on gram positive cells (PAMPS)
b. Exotoxins are released outside the producing cell (more acute)
i. A-B toxins: B subunits binds to host cell receptor
1. A subunit has a negative action inside the cell (the effector portion)
ii. Cytolysins: Act on cell membranes – lysis of cells – often act on red blood cells to
release iron
iii. Superantigens: nonspecifically stimulate T cells to secrete large amounts of cytokine
1. superantigens get presented on a MHC II which results in a large immune
response that = self damage
6.) What are the effects of LPS and LTA on the host?
a. Evokes inflammatory response in the host.
7.) Describe/diagram how A-B toxins work and give as many examples for different modes of
action as possible.
a. A portion- has enzymatic activity. B- portion attaches to the receptor on the host.
 b.
8.) How do cytolysins work and how is this beneficial to the bacteria? Draw an example of
cytolysin acting on a host cell membrane
a. Work on plasma membranes of cells, often forming pores or degrading phospholipids
b. Require host receptors to lead to a conformational change and insertion of hydrophobic
segments into a membrane  forms a pore
c. Hemolysins are a classic example, lysing red blood cells
i. For iron acquisition
d. Lysing cells for interior nutrients
9.) How do superantigens work? Draw out the cellular interactions that are occurring with
superantigens and indicate how this is different from normal cell interactions and antigen
presentation.
a. Exotoxins that act on helper t cells
b. Cause a massive release of nonspecific cytokines
 c. Induce a systematic inflammatory response
10.) Describe 3 ways in which bacteria deliver or release virulence factors
a. Cell lysis
b. Secretion to environment
c. Injection into host
11.) What are capsules? Describe/draw how they act as potent virulence factors. How can capsule
recognition lead to autoimmunity?
a. Extracellular loose matrix of polysaccharides
b. Provide attachment and immune evasion mechanisms for pathogens
i. Blocks opsonization, interfering with phagocytosis
ii. Blocks antibody/complement
iii. Reduced entry into endocytic pathway lessens antigen presentation
iv. Mimics “self” molecules, preventing stimulation of antibody/complement responses
12.) What are the various ways in which bacteria acquire iron in the host?
a. Siderophores= iron-binding molecules that compete with host iron-binding proteins
b. Lowering pH at the site of infection, impairing host iron-binding protein activities
c. Production of cytolysins that lyse host cells to get their iron stores
13.) Describe the different virulence factors of S. pyogenes. How can each of these virulence factors
lead to disease in the host? Describe the different types of diseases caused by the bacterium
a. Access to host tissues – attachment factors
i. Fimbriae that attach to fibronectin and collagen
ii. Physical damage can allow direct access to deeper tissues
b. Overcoming host defenses
i. Capsules- prevent phagocytosis
ii. Capsules inhibit antibody/complement binding
iii. M proteins can bind antibodies by the Fc region
iv. Collectively these deter immune responses long enough for the pathogen to expand its
population
14.) How does S. pyogenes gain access to host tissues?
a. ^
15.) How does Mycobacterium tuberculosis gain access to host tissues?
a. Spread by inhalation of aerosols from infected individuals
b. Bacterium replicates inside phagosomes of lung macrophages
i. This protects the cells from complement-mediated lysis and antibodies
ii. The bacteria actually encourage phagocytosis via opsonization with complement
proteins C3b and mannose binding lectin
16.) How does M. tuberculosis avoid host defenses?
a. Elimination of the microbe is mediated by T helper cell responses and upregulation of
macrophage killing functions
b. Preventing phagosome fusion with lysosomes keeps bacteria alive in lung macrophages
c. Bacteria also produce and surround themselves with LAM
i. Downregulates oxidative bursts
ii. Neutralizes many toxic oxygen species
17.) Diagram the ways in which M. tuberculosis causes disease and how the immune system of the
host is an important determiner of disease.
 a.
18.) How does the TB skin test work? Why is a follow-up chest x-ray needed for positive or
equivocal results?
a. For granulomas
b. Previous exposure to the microbe results in a cell mediated immune reaction

Chapter 21: Viral Pathogenesis

1.) What is the difference between a productive and an abortive viral infection?
a. Productive – new infectious viral particles produced
b. Abortive- few if any new viral particles are produced
2.) What is an acute infection?
a. Short duration, signs/symptoms observed, infection is cleared (immunity usually results) –
like a common cold
3.) What is a latent infection? Describe the process of lysogency/latency in phages and
herpesviruses
a. Period of acute infection is followed by latency
i. Virus is still present, but replication is shut down
b. Reactivation may occur, leading to recurrence of acute infection signs and symptoms
c. They are not actively replicating it is incorporated into the DNA
d. Herpesvirus maintains a circular episome during latency
4.) How are chronic infections different from latent infections?
a. New viral particles are continuously produced
i. The host doesn’t clear the virus, but signs and symptoms may cease.
ii. Hep B and Hep C
5.) Describe the different types of transmission mechanisms among hosts for viruses, and give
example viruses that are transmitted via each of those mechanisms.
a. Horizontal – human to human- requires a mode of exit and a mode of entry
i. Respiratory, fecal-oral, sexual –rhinovirus- cold, poliovirus, HIV
b. Vertical
i. Mother to fetus transmitted through the placenta or during birth or via breast milk
c. Zoonotic- transmission from a non-human host to humans
i. Rabies
d. Mechanical/vector
i. Facilitated transfer of virus from host to host via another vector
 1. Aka mosquito which is not a host but just a transmission route
6.) How is necrosis different from apoptosis? Describe/diagram cellular processes that are
affected
a. Necrosis- the cell bursts sometimes due to overfilling the cell with new viruses
i. Other times, due to viral impairment of normal cell functions
ii. Inhibits host translation 2 ways
1. 5’ cap stealing
b. Apoptosis- programmed cell death
i. A more subtle death, safer for surrounding cells
ii. Cell “commits suicide”
1. Internal events occur that degrade DNA into small fragments
2. Bits of cell are released as “blebs”
3. This typically does not induce inflammation
4. Induction of apoptosis is used by our immune system to safely kill virally
infected cells.
7.) What are syncytia bodies and inclusion bodies and how can these potentially promote viral
persistence?
a. Some viruses can fuse host cells together, forming syncytia that often kill the cells.
i. By doing so, they can avoid extracellular immune responses.
b. Other viruses may form clumps of virus/proteins inside host cells (inclusion bodies) that
often kill cells.
8.) Give examples of how the host immune response against a virus can lead to disease symptoms
more so than just the effect of the virus on its own.
a. Example the common cold- on top of the normal symptoms we have the inflammatory
cytokines that make symptoms worse
b. Hep B- immune response is to kill off infected hepatocytes (liver cells) this is what leads to
death
i. Hepatocytes not actually fatal, but the immune response is.
c. If molecular mimicry occurs, an antiviral response accidentally views self structures as
foreign.
9.) How can viruses cause cancer? Give examples.
a. Transformation events produce changes in a cell that make it cancer-like
i. Some viruses possess oncogenes, genetic material capable of inducing transforming
events in host cells.
ii. Tumorigenesis may result from a viral protein inducing a normally quiescent (not
dividing) cell to enter the cell cyle
10.) What 3 events/mechanisms can lead to viral evolution? Describe each in detail
a. Mutations
i. Viruses lack proofreading activity of DNA polymerase. This can lead to changes in
the virus over time, which can complicate treatments, can change which cells are
infected in a persistent infection
b. Virus recombination
i. Fusion of pieces of two separate viral genomes to create a new hybrid genome
ii. Can result in entirely new properties rapidly
1. Polymerase moves onto another template during synthesis
c. Virus reassortment
1. When multiple viruses with segmented genomes infect the same cell they can
swap segments in newly formed virus
a. This can lead to new or modified virulence trains

11.) How did the H1N1 influenza strain come about? Why do you think this caused a pandemic?
 a. Coinfection of one pig which was then exposed to humans and these things have never been
exposed to humans.

Chapter 22: Control of Infectious Disease

1.) What is the difference between an antimicrobial drug, an antiseptic, and a disinfectant?
a. Antimicrobial drug are administered internally and have selective toxicity – more toxic to
viral cell
b. Antiseptic- cleaning wounds
c. Disinfectants- sterilize inanimate objects
2.) Give a basic summary of the history of antibiotic drug production, and the development of
resistance against antibiotics.
a. It’s a cycle of introduction and resistance. It is a constant battle to create new antibiotics.
Long term usefulness of antibiotics are limited.
3.) Give an example of 3 antibiotics that were named after the species that produced them.
a. Penicillin, streptomycin bacitracin
4.) What are the 6 main mode of actions of antibiotics?
a. Peptidoglycan synthesis
b. Membrane integrity
c. DNA synthesis
d. Transcription
e. Folic acid synthesis
f. Ribosome function
5.) How do inhibitors of peptidoglycan synthesis work? Why do they only work on certain classes
of bacteria?
6.) How do inhibitors of ribosomal function work? Be specific.
7.) What are the common mechanisms of action of antifungal drugs? Give examples.
8.) What tare the common mechanisms of action of antiprotozoal drugs? Give examples.
9.) How do microbes develop resistance to drugs? Be specific.
10.) What are several specific ways that we can reduce or limit antimicrobial drug resistance?
11.) What is herd immunity and how does it impact a population’s protection against major
epidemic diseases?