Exam II Flashcards

1
Q

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?

A
  • sporozoites are the infective stage that’s found in the mosquito
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2
Q

Of the 4 species of Plasmodium that infect humans, which shows the greatest prevalence?

A
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3
Q

Of the 4 species of Plasmodium that infect humans, which shows the lowest prevalence?

A
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3
Q

What is the prevalence of malaria?

A
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4
Q

what is the incidence of malaria?

A
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5
Q

what is the annual mortality of malaria?

A
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6
Q

what is the malaria vector?

A
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7
Q

How does the malaria vector introduce the parasite into the body?

A
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8
Q

Once sporozoites enter the bloodstream (in malaria), which cells do they infect first?

A
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9
Q

Once sporozoites enter the bloodstream (in malaria), by what indirect process do they arrive at their final destination cell?

A
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10
Q

What stage of the vertebrate life cycle is this called in malaria?

A
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11
Q

In what form do merozoites enter the bloodstream in malaria?

A
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12
Q

Of the 4 human-infecting species, which produces the most merozoites in the shortest period of time?

A
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13
Q

Define hypnozoite.

A
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14
Q

In which species of malaria does hypnozoite occur?

A
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15
Q

What is the clinical significance of a hypnozoite?

A
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16
Q

What is the definition of relapse?

A
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17
Q

What are the events during invasion of a red blood cell by a merozoite (in malaria)?

A
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18
Q

what is meant by a moving junction (in malaria)?

A
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19
Q

What stage of the vertebrate life cycle does the moving junction begin?

A
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20
Q

Can merozoites re-infect liver cells?

A
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21
Q

Are all stages of red blood cells equally susceptible to invasion by all species?

A
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22
Q

Which species prefers which RBC stage?

A
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23
Q

How does the preference of RBC cells explain the observed levels of parasitemia that develop in the different species?

A
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24
What are the stages of development that the parasite undergoes in the red blood cell in malaria?
25
what are the morphological features associated with each stage in malaria?
26
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?
27
What is hemozoin?
28
Why does P. falciparum seemingly “disappear” from the peripheral blood at a particular stage, and what advantage does the parasite gain?
29
Why is the disappearance of P. falciparum from the peripheral blood a problem for the patient?
30
9. Which species produces the most merozoites from red blood cells in the shortest time (in malaria)?
31
What is the explanation for the periodic chills and fever associated with malaria?
32
What is the timing of the periods for each of the 4 human-infecting species of malaria?
33
What is recrudescence?
34
which species demonstrates recrudescence?
35
How does recrudescence differ from relapse?
36
What two paths of development can the merozoite undergo (in malaria)?
37
What stage indicates the beginning of gametogony?
38
Where are gametes finally formed (in malaria)?
39
Why is microgametogenesis referred to as “exflagellation?”
40
Where does sporogony occur?
41
what developmental stages are involved in sporogony?
42
what is the final product of sporogony?
43
What is the complete life cycle of Plasmodium, including all stages of development in both the mosquito and human host?
44
In which host does gametogony begin, and in which host is it concluded?
45
What are the main symptoms of malaria?
46
In which groups are the symptoms worst in malaria?
47
What causes the high fever in malaria?
48
Why do malaria patients show marked anemia?
49
What is the complication caused by P. malariae and what is the mechanism?
50
What are the complications specifically associated with malaria caused by P. falciparum?
51
Which is the most dangerous complication of malaria caused by P. falciparum?
52
What is a possible consequence of the severe immunosuppression caused by P. falciparum?
53
What genetic traits are found in people living in certain P. falciparum transmission areas?
54
What genetic traits are found in people living in certain in certain P. vivax transmission areas?
55
18. What is the evidence for immune protection during initial infection?
56
What is the evidence that protective immunity against reinfection actually occurs against malaria?
57
What type of immunity is the protective immunity (e.g., compared to sterile immunity induced by the polio vaccine)?
58
How do the malaria parasites in general avoid the immune response, and what special strategy is used by P. falciparum?
59
What are the harmful effects of the immune response on the host?
60
How is malaria diagnosed, and why is P. falciparum at times particularly difficult to diagnose?
61
What are the strategies for preventing disease if a person is going to travel to a malarious area?
62
If you are about to travel to a malarious area, how would you determine current chemotherapeutic and treatment medications?
63
Why was it believed after WWII that malaria was on the verge of being eradicated? What happened to dash this hope?
64
What is the current control strategy of malaria in Africa?
65
How does the parasitology of Babesia differ from that of Plasmodium?
66
Of what veterinary significance is babesiosis?
67
What species cause infections in humans, where are these infections most prevalent in the US, and what are the health consequences?
68
Are there any patients at high risk for fatal babesiosis?
69
why is Plasmodium falciparum one of humanity’s greatest scourges?
70
What are the key morphological features that distinguishes amoebae?
71
What is the function of the cyst stage in parasitic amoebae?
72
Is Entamoeba histolytica of minor or major health significance worldwide, and why?
73
Why is the worldwide prevalence of infection with E. histolytica difficult to estimate?
74
In what 2 morphological forms does E. histolytica occur during its life cycle?
75
Where do you find the trophozoite of E. histolytica in humans?
76
In what type of stools is the trophozoite of E. histolytica in humans seen, and why?
77
What stimulates the trophozoite to encyst (in amoebas)?
78
What are the 3 stages of encystation and what are the morphological features of each stage (in amoebas)?
79
Which stage of encystation is most common in stools (in amoebas)?
80
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?
81
How frequently is disease associated with infection in the case of E. histolytica?
82
What specific event is associated with disease in the case of E. histolytica?
83
What are some of the factors that could result in disease of E. histolytica?
84
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?
85
What is the histological appearance of an area of tissue invasion by E. histolytica?
86
What is the range of symptoms that occurs in amoebiasis?
87
What factor determines whether mild or severe symptoms occur in amoebiasis?
88
What are some of the complications that can occur in the colon in amoebiasis?
89
What are some of the complications that can occur if amoebae enter the bloodstream?
90
Why is it difficult to rule out E. histolytica as a cause of gastrointestinal disease?
91
What is the crystal that is often present in the stool of patients with colon infections, and what is the source of this crystal?
92
Why is extraintestinal amoebiasis even more difficult to diagnose?
93
Where is Naegleri fowleri normally found in nature?
94
Why is N. fowleri considered a facultative parasite?
95
What additional stage is found in the life cycle of N. fowleri that doesn’t occur in that of E. histolytica?
96
What is the infective stage of N. fowleri?
97
What environmental factor causes numbers of the infective stage to increase in N. fowleri?
98
How do humans commonly become infected with N. fowleri?
99
What is the name of this disease that invariably results, and what is the outcome of N. fowleri?
100
Where are Acanthamoeba spp. normally found in nature?
101
What stages occur in Acanthamoeba spp. life cycle?
102
Which is the infective stage of Acanthamoeba spp.?
103
In histological sections of infected tissue, what difference would immediately distinguish Acanthamoeba from Naegleria or E. histolytica?
104
Where do infections occur in immunocompetent persons?
105
how are immunocompetent persons typically acquired?
106
what are the pathological effects in immunocompetent persons?
107
are immunocompetent persons easy to treat?
108
Where do infections occur in immunodeficient persons?
109
how are immunodeficient persons typically acquired?
110
what are the pathological effects of immunodeficient persons?
111
Are immunodeficient persons easy to treat?
112
What is the name of the disease that results when Acanthamoeba reaches the brain, and what is the outcome?
113
what's the role in Legionnaire’s disease?
pneumoniae?
114
How do human infections with with Naegleria compare with Acanthamoeba infections, in terms of risk factors, disease caused, and cyst formation in the tissues?
115
What organelle that occurs in most types of eukaryotic cells is missing in this group, and what is the evolutionary significance of this observation?
115
What are the 2 stages in the life cycle of Giardia lamblia?
116
what are the main structural features of each stage of Giardia lamlia?
117
Where in the host is the trophozoite of G. lamblia normally found?
118
How does the trophozoite of G. lamblia adhere to the host surface?
119
In what type of stools does the trophozoite of G. lamblia occur?
120
What is the function of the cyst stage of G. lamblia, and why is it better suited for this function than the trophozoite?
121
How do humans become infected with Giardia lamblia?
122
What are the environmental cues that trigger encystation and excystation of G. lamblia?
123
Does G. lamblia invade the tissues?
124
In which group of patients does giardiasis seem to be worst?
125
What histological change in the intestine sometimes accompanies severe giardiasis?
126
Does infection with G. lamblia invariably lead to disease?
127
If disease occurs with the infection of G. lamblia, what are the symptoms?
128
What is malabsorption syndrome?
129
Where is giardiasis endemic and where is it epidemic?
130
Where are “hot spots” of transmission in the US?
131
Why is giardiasis sometimes contracted in pristine wilderness areas?
132
How easy is it to diagnose infection with G. lamblia?
133
What special techniques are used for diagnosis of G. lamblia?
134
What drug is routinely prescribed for giardiasis?
135
What is the potential risk associated with the drug prescribed for giardiasis?
136
What is the significance of nonpathogenic parasites, i.e., why bother studying them?
137
What is the difference between a false positive and a false negative diagnosis? Which is potentially more harmful?
138
What life cycle characteristic do all trichomonads share?
139
What are the main structural features of a trichomonad?
140
Where is Trichomonas vaginalis found in humans and how does it get there?
141
What are the symptoms of infection with T. vaginalis in men and women?
142
What is the drug treatment for infection of T. vaginalis?
143
To what other infection does trichomoniasis make persons more susceptible?