BIOL 305 Exam 2: Midterm Study Guide (2024)
Dr. Gillen, Updated 3/1/2024
The BIOL 305 Midterm is mildly cumulative but mainly emphasizes Protozoan parasites
since the last exam. It is 52 questions in objective (TopHat) format. It includes Multiple
Choice, True-False, Matching, and a several questions on malaria. The 25 questions
quiz before spring break is completely on malaria. I am including some questions to
ponder in this document and a second document (PDF) that gives practice questions.
Exam 2 has a few questions on each parasite type from the Giardia parasites through
malaria. The more detailed questions on malaria after break on the Malaria quiz. Know
all the basics for malaria (including the Return of Malaria to the USA) as well as the
introductory part for the in-depth. Malaria species details on the malaria quiz, as well as
details of life cycle and origins. Know infective vs. diagnostic stages for major diseases.
Exam 2 will have many questions on amoebas, Cryptosporidium, and diagnostics (via
stool, blood, DNA, etc.) of the various protozoan parasites (a matching section).
Questions in the Lab manual on the Genesis of Malaria reading will help more on the
malaria quiz: the week after Spring break.
What should I know from this section?
Lumen Dwelling Flagellates (ex. Giardia)
Focus on: comparisons, infectious/diagnostic stage
1. What organelle that occurs in most types of eukaryotic cells is missing in this group,
and what is the evolutionary significance of this observation?
2. What are the 2 stages in the life cycle of Giardia lamblia, and what are the main
structural features of each stage?
3. Where in the host is the trophozoite of G. lamblia normally found? How does it
adhere to the host surface? In what type of stools does the trophozoite occur?
4. What is the function of the cyst stage of G. lamblia, and why is it better suited for this
function than the trophozoite? How do humans become infected?
5. What are the environmental cues that trigger encystation and excystation of G.
lamblia?
6. Does G. lamblia invade the tissues? In which group of patients does giardiasis seem
to be worst? What histological change in the intestine sometimes accompanies severe
giardiasis?
7. Does infection with G. lamblia invariably lead to disease? If disease occurs, what are
the symptoms? What is malabsorption syndrome?
8. Where is giardiasis endemic and where is it epidemic? Where are “hot spots” of
transmission in the US? Why is giardiasis sometimes contracted in pristine
wilderness areas?
9. How easy is it to diagnose infection with G. lamblia? What special techniques are
used for diagnosis of this parasite?
10. What drug is routinely prescribed for giardiasis? What is the potential risk associated
with this drug?
11. What is the significance of nonpathogenic parasites, i.e., why bother studying them?
What is the difference between a false positive and a false negative diagnosis? Which
is potentially more harmful?
12. What life cycle characteristic do all trichomonads share? What are the main
structural features of a trichomonad?
13. Where is Trichomonas vaginalis found in humans and how does it get there?
14. What are the symptoms of infection with T. vaginalis in men and women? What is the
drug treatment for infection? To what other infection does trichomoniasis make
persons more susceptible?
Carl Fliermans; Legionnaire’s disease; role of amoeba in spread of disease;
alveolar macrophages; invasive vs. infective stages vs. diagnostic stages.
Amoebae
1. What are the key morphological features that distinguishes amoebae?
a. No form-retaining pellicle, flexible plasma membrane, clear ectoplasm,
and granular endoplasm
b. Use pseudopods for locomotion and feeding
2. What is the function of the cyst stage in parasitic amoebae?
a. It is the transmission stage
3. Is Entamoeba histolytica of minor or major health significance worldwide, and why?
Why is the worldwide prevalence of infection with E. histolytica difficult to estimate?
In what 2 morphological forms does it occur during its life cycle?
a. It is a major health significance worldwide because it causes 50 million
infections and has 500 million carriers
b. It Is difficult to estimate because 90% of people are asymptomatic
c. It occurs as a cyst or trophozoite
4. Where do you find the trophozoite of E. histolytica in humans? In what type of stools
is it seen, and why?
a. You find the trophozoite of e. histolytica in humans in the colon
b. It is not found in formed stools due to encystation
5. What stimulates the trophozoite to encyst? What are the 3 stages of encystation and
what are the morphological features of each stage? Which stage is most common in
stools?
a. Trophozoites are stimulated to encyst by dehydration of feces in the colon
b. The 3 stages of encystation are
i. Precyst
1. Food exocytosed, round shape, and chromatoidal bars
ii. Cyst
1. Clear, proteinaceous cyst wall
iii. Metacyst
1. 4 nuclei
2. Most common stage in stools!
6. What type of cell emerges from the metacyst when it is ingested and reaches the
duodenum? How many daughter cells are produced initially by this cell?
a. Quadrinucleate emerges
b. 8 metacystic trophozoite
7. How frequently is disease associated with infection in the case of E. histolytica?
What specific event is associated with disease? What are some of the factors that
could result in disease?
a. 90% of infections are asymptomatic
b. Amebiasis is associated with e. histolytica
c. Factors
i. Pathogenic strain of amoeba
ii. Decreased mucosal immunity
iii. Abnormal bacterial flora
8. What is the mechanism by which E. histolytica is able to invade tissues and then is
able to avoid being killed by white blood cells? What is the histological appearance
of an area of tissue invasion by E. histolytica?
a. Amebiasis, invasion occurs through pore puncturing chemical, once
punctures, the chemicals are released
b. Appearance: lysis of epithelial cells, bleeding, flask-shaped ulcer
9. What is the range of symptoms that occurs in amoebiasis? What factor determines
whether mild or severe symptoms occur? What are some of the complications that
can occur in the colon? What are some of the complications that can occur if
amoebae enter the bloodstream?
a. Symptoms:
b. Factors: strain, persons immune response, dosage of infection, number of
amoebas
10. Why is it difficult to rule out E. histolytica as a cause of gastrointestinal disease?
What is the crystal that is often present in the stool of patients with colon infections,
and what is the source of this crystal? Why is extraintestinal amoebiasis even more
difficult to diagnose?
a. It has similar structure to other amoebae
11. Where is Naegleri fowleri normally found in nature? Why is N. fowleri considered a
facultative parasite? What additional stage is found in the life cycle of N. fowleri that
doesn’t occur in that of E. histolytica? What is the infective stage? What
environmental factor causes numbers of the infective stage to increase? How do
humans commonly become infected? What is the name of this disease that invariably
results, and what is the outcome? Explain the genesis of the brain-eating amoeba.
a. Naegleria fowleri found in soil and fresh water
b. Facultative because it is free living and does not require a host
c. Biflagellated form
d. Warm water temps
e. Injestion through swimming, diving, neti pots – through nasal cavity
f. Genesis: how do we think it originaaly started
12. Where are Acanthamoeba spp. normally found in nature? What stages occur in its
life cycle? Which is the infective stage? In histological sections of infected tissue,
what difference would immediately distinguish Acanthamoeba from Naegleria or E.
histolytica? Where do infections occur in immunocompetent persons, how are they
typically acquired, what are the pathological effects, and are they easy to treat? What
is the name of the disease that results when Acanthamoeba reaches the brain, and
what is the outcome? Role in Legionnaire’s disease; pneumoniae
a. Acanthamoeba spp. Found in soil
b. Cyst and trophozoite
c. Pseudopods with spikes
d. Infections occur in the eyes, not typically acquired, difficult to treat
e. GAE – if reaches the brain
f. Ancanthamoeba is hyperparasitized by legionella pneumophila
13. How do human infections with with Naegleria compare with Acanthamoeba
infections, in terms of risk factors, disease caused, and cyst formation in the tissues?
a.
14. Matching section on amoebas with basic cell features – diagnostic stages.
Apicomplexa
1. What structural feature is shared by both apicomplexans and amoebas?
a. Endosome
2. What is the usual infective stage (for vertebrates) in the apicomplexan life cycle?
The defining feature of the phylum Apicomplexa is the apical complex. What is
the function of this complex, what are its components, and what is the function of
each? With what structure do apicomplexans obtain their food?
a. Oocyst
b. Degenerative chloroplast – function?
c.
3. What are the 3 stages in the life cycle of a “typical” apicomplexan? Which stage
would you expect to cause the most tissue destruction?
a.
4. Define schizogony (merogony). How does this process differ from typical mitotic
cell division? What is the intracellular stage that gives rise to the schizont? What
are the daughter cells called?
a. Asexual production of merozoites
b. Daughter cells = merozoites
5. What 2 stages are involved in sexual reproduction in Apicomplexa (or for that
matter, any sexually-reproducing organism)? What is the intracellular stage that
gives rise to the gametes? What 2 types of gametes are formed, and how do they
differ in terms of size and number?
a.
6. Once the zygote is formed, what type of cell division does it then undergo? What
daughter cells are initially formed, and what do these in turn produce?
7. In the apicomplexan life cycle, which stages are haploid, and which are diploid?
8. In which two classes are all of the medically important apicomplexans found?
What 3 general life cycle strategies (occurrence of intermediate host, location of
schizogony) are employed by these pathogens?
9. How does the oocyst of Cryptosporidium parvum differ from that of the above
apicomplexans? Does it require a period of time outside of the host to sporulate?
What rather unusual part of the intestinal epithelial cell does this parasite infect?
10. During schizogony of C. parvum, what 2 types of meronts are formed, and what is
the fate of each? What is the pathological effect in immunocompetent and
immunodeficient persons? Why might it have been profitable to have cornered
the market on toilet paper in Milwaukee in 1993? Is cryptosporidiosis treatable?
Blood Apicomplexa (Most important)
Know: basics powerpoint
New for Malaria quiz; not Exam 2
Malaria – sickle cell/malaria connection with critical thinking questions
https://www.hhmi.org/biointeractive/making-fittest-natural-selection-
humans
What is the “malaria attack”? benign malaria? Malignant malaria? What are
complications of malaria?
WHAT SHOULD I KNOW FROM THIS SECTION
1. What 3 characteristics do members of the Plasmodiidae have in common, relative to
their sporozoite, type of life cycle, and location of each phase of the cycle? Of the 4
species of Plasmodium that infect humans, which shows the greatest and which
shows the lowest prevalence?
2. What is the prevalence, incidence, and annual mortality of malaria?
3. What is the malaria vector? How does the vector introduce the parasite into the
body?
4. Once sporozoites enter the bloodstream, which cells do they infect first, and by what
indirect process do they arrive at their final destination cell? What stage of the
vertebrate life cycle is this called? In what form do merozoites enter the bloodstream?
5. Of the 4 human-infecting species, which produces the most merozoites in the shortest
period of time?
6. What is a hypnozoite, in which species does it occur, and what is its clinical
significance? What is the definition of relapse?
7. What are the events during invasion of a red blood cell by a merozoite, and what is
meant buy a moving junction? What stage of the vertebrate life cycle does this
begin? Can merozoites re-infect liver cells? Are all stages of red blood cells equally
susceptible to invasion by all species? Which species prefers which RBC stage?
How does this preference explain the observed levels of parasitemia that develop in
the different species?
8. What are the stages of development that the parasite undergoes in the red blood cell,
and what are the morphological features associated with each stage? What are some
of the key morphological features that allow you to distinguish one species from
another, e.g., morphology of the trophozoite, presence or absence of Schuffner’s dots,
appearance of infected red blood cell? What is hemozoin? Why does P. falciparum
seemingly “disappear” from the peripheral blood at a particular stage, and what
advantage does the parasite gain? Why is this disappearance a problem for the
patient?
9. Which species produces the most merozoites from red blood cells in the shortest
time?
10. What is the explanation for the periodic chills and fever associated with malaria?
What is the timing of the periods for each of the 4 human-infecting species?
11. What is recrudescence, which species demonstrate it, and how does it differ from
relapse?
12. What two paths of development can the merozoite undergo? What stage indicates the
beginning of gametogony? Where are gametes finally formed? Why is
microgametogenesis referred to as “exflagellation?”
13. Where does sporogony occur, what developmental stages are involved, and what is
the final product?
14. What is the complete life cycle of Plasmodium, including all stages of development in
both the mosquito and human host? In which host does gametogony begin, and in
which host is it concluded? You should be able to diagram the life cycle and make
simple drawings of the different developmental stages.
15. What are the main symptoms of malaria? In which groups are the symptoms worst?
What causes the high fever? Why do malaria patients show marked anemia? What is
the complication caused by P. malariae and what is the mechanism?
16. What are the complications specifically associated with malaria caused by P.
falciparum? Which is the most dangerous complication? What is a possible
consequence of the severe immunosuppression caused by P. falciparum?
17. What genetic traits are found in people living in certain P. falciparum transmission
areas? In certain P. vivax transmission areas?
18. What is the evidence for immune protection during initial infection? What is the
evidence that protective immunity against reinfection actually occurs against malaria?
What type of immunity is this (e.g., compared to sterile immunity induced by the
polio vaccine)?
19. How do the malaria parasites in general avoid the immune response, and what special
strategy is used by P. falciparum?
20. What are the harmful effects of the immune response on the host?
21. How is malaria diagnosed, and why is P. falciparum at times particularly difficult to
diagnose?
22. What are the strategies for preventing disease if a person is going to travel to a
malarious area? If you are about to travel to a malarious area, how would you
determine current chemotherapeutic and treatment medications?
23. Why was it believed after WWII that malaria was on the verge of being eradicated?
What happened to dash this hope? What is the current control strategy in Africa?
24. How does the parasitology of Babesia differ from that of Plasmodium? Of what
veterinary significance is babesiosis? What species cause infections in humans,
where are these infections most prevalent in the US, and what are the health
consequences? Are there any patients at high risk for fatal babesiosis?
25. Taking everything (e.g., prevalence, biotic potential, pathological effects, immune
interaction, diagnosis, treatment, prevention) into consideration, why is Plasmodium
falciparum one of humanity’s greatest scourges?
