Test 2 (week 2)

Question 1

What is the best known pathogenic yeast?

Answer 1

Candida albicans. Candida is in the gastrointestinal and vaginal microbiomes (normal flors)

Question 2

causes lung infections that often spread to the skin and central nervous system.

Answer 2

Cryptococcus neoformans

Question 3

eukaryotic single-cell organisms (protozoa) or complex multi-cellular organosms (Helminths)

Answer 3

parasites

Question 4

either single cell organisms (typically yeast) or complex multi-cellular forms (mold)

Answer 4

fungi

Question 5

typically form thread-like hyphae and usually form conidia (spores)

Answer 5

molds

Question 6

tapeworms made up of an attachment end (scolex) with many, many segments (proglottids)

Answer 6

cestodes

Question 7

roundworms

Answer 7

nematodes

Question 8

leaf-shaped flukes that infect the gastrointestinal tract.

Answer 8

trematodes

Question 9

How are filoviruses transferred?

Answer 9

Filoviruses are transmitted through direct contact with blood or bodily fluids (saliva, sweat, feces, urine, vomit, breast milk, and semen).

Question 10

Filoviruses initially infect _____.

Answer 10

macrophages and dendritic cells

Question 11

How do filoviruses typically enter human populations?

Answer 11

Filoviruses typically enter human populations by handling bushmeat (wild animals hunted for food) and contact with infected bats

Question 12

where do you typically see yellow fever today?

Answer 12

Today, yellow fever is found primarily in subtropical areas of Africa and South America

Question 13

What carries yellow fever to humans?

Answer 13

mosquitos

Question 14

How does the Hantavirus get to humans?

Answer 14

Hantaviruses cause persistent infections of rodents and may cause disease in humans following transmission through aerosolized excreta

Question 15

What are the two most common species of plasmodium that infect humans?

Answer 15

P. falciparum

P. vivax

Question 16

describe the Exoerythrocytic stage (1st stage) in plasmodium life cycle

Answer 16

** no symptoms of disease are seen in this stage**
Sporozoites introduced at bite site in mosquito saliva–>
Infects hepatocytes and undergoes asexual replication
(Product of replication are merozoites)

Question 17

Describe the erythrocytic stage (second stage) in plasmodium life cycle.

Answer 17

Merozoites infect red blood cells (RBCs).
Asexual replication occurs in RBCs.
-Ring-stage (Early Trophozoites)

-Late Trophozoites
-Schizonts
Some merozoites develop into male and female gametocytes within RBCs

this stage is where you see clinical manifestations

Question 18

What causes the cyclic fever spikes in plasmodium infections?

Answer 18

spikes occur when RBCs are lysed by parasites

Question 19

The quartan fever cycle is characteristic of ____.

Answer 19

malaria

Question 20

The tertian fever cycle is characteristic of _____.

Answer 20

P. falciparum

P. vivax

Question 21

how are plasmodium parasites transmitted to humans?

Answer 21

Transmitted through the bite of a female Anopheles mosquito

Question 22

What is the treatment plan for plasmodium vivax?

Answer 22

P. vivax – give chloroquine and then primaquine

Question 23

What is the treatment plan for plasmodium falciparum (poses greatest risk of mortality)?

Answer 23

pretty much anything but chloroquine

Question 24

describe positive polarity RNA viruses.

Answer 24

• viral RNA genome directly serves as mRNA

- synthesizes viral encoded transcriptase

Question 25

Describe negative polarity RNA viruses.

Answer 25

- Viral RNA genome CANNOT serve as mRNA - Viral RNA transcriptase must be included within virion - The transcriptase copies genomic RNA into complementary positive-sense mRNA that is used to synthesize viral proteins

Question 26

Where does viral RNA replication occur?

Answer 26

cytoplasm

Question 27

Where does viral DNA replication occur?

Answer 27

nuclues

Question 28

Which RNA virus is not replicated in the cytoplasm?

Answer 28

influenza--> happens in nucleus

Question 29

Which DNA virus is not replicated in the nucleus?

Answer 29

poxvirus--> happens in cytoplasm

Question 30

What is the MOA of Acyclovir (and other herpes drugs for that matter)?

Answer 30

are analogs of nucleosides that prevent DNA chain elongation

Question 31

What are the prototype herpes drugs?

Answer 31

Acyclovir

Question 32

Which is metabolized in the liver: NRTIs or NNRTIs?

Answer 32

NNRTIs; because of this, you can see drug interactions

Question 33

What are the different classes of drugs used to treat HIV?

Answer 33

NRTIs, NNRTIs, protease inhibitors, and entry inhibitors

Question 34

What is the mechanism of action of NRTIs?

Answer 34

NRTIs are analogs of nucleosides but lack a 3’ hydroxyl group -->Attachment of the next nucleotide is impossible

Question 35

What is the mechanism of action of NNRTIs?

Answer 35

bind to site on viral transcriptase and prevent further RNA to DNA synthesis

Question 36

What is the mechanism of action of protease inhibitors?

Answer 36

inhibit the HIV proteases needed to assemble the coat structures correctly

Question 37

What is the mechanism of action of entry inhibitors?

Answer 37

Attachment of many HIV strains requires two receptors on human cells Drugs bind to this receptor or the proteins that can block attachment and entry of HIV into the cell

Question 38

What are the prototype NRTIs?

Answer 38

Abacavir, Didanosine, Lamivudine

Question 39

What are the prototype NNRTIs?

Answer 39

Efavirenz, Nevarapine

Question 40

What are the prototype protease inhibitors?

Answer 40

Retonavir, Atazanavir

Question 41

What are the prototype entry inhibitors?

Answer 41

Miravoc, Enfuvirtide

Question 42

What is the prototype CMV drug?

Answer 42

Ganciclovir

Question 43

What are the general adverse effects of NRTIs?

Answer 43

Lactic acidosis producing: | Hepatomegaly, steatosis (higher fat storage in cells)

Question 44

What are the general adverse effects of NNRITs?

Answer 44

multiple drug interactions since it is degraded in the liver

Question 45

What are the general adverse effects of Protease inhibitors?

Answer 45

-Use in HAART has led to carbohydrate and lipid metabolism disorders -Cross-inhibits endogenous lipid-regulating proteins -Leads to altered body fat disposition “buffalo hump” and gynecomastia -Hyperglycemia and insulin resistance

Question 46

What is the MOA of Amantadine and Rimantadine?

Answer 46

Block the M2 proton ion channel of the virus -Inhibits uncoating of the virus in cells Thus preventing replication

Question 47

What are the adverse effects of Amantadine and Rimantadine?

Answer 47

GI, dizziness, slurred speech

Question 48

What are the primary influenza drugs?

Answer 48

Oseltamivir, Zanamivir

Question 49

What are the primary Hepatitis drugs?

Answer 49

Interferon-alpha, Ribavirin

Question 50

What is the MOA for Oseltamivir and Zanamivir

Answer 50

- Inhibit neuraminidase A and B | - Reduce viral spreading

Question 51

What is the MOA for interferon-alpha?

Answer 51

- Host cytokine that exerts complex antiviral, immunomodulatory and antiproliferative actions - Enhances phagocytic activity of macrophages - Augmentation of the proliferation and survival of cytotoxic T cells.

Question 52

What are the adverse effects of interferon-alpha?

Answer 52

``` GI irritation flu-like syndrome fatigue severe depression alopecia thyroid dysfunction mental confusion ```

Question 53

What is the MOA for Ribavirin?

Answer 53

Prodrug – when active, represents RNA nucleotide; Inhibits GTP formation, mRNA capping, and block RNA-dependent polymerases IT MUST BE USED WITH ANOTHER ANTIVIRAL DRUG, DOES NOT LIKE BEING ALONE

Question 54

What are the adverse effects of ribavirin?

Answer 54

hemolytic anemia