Block 4: Antiparasitic-Blood And Tissue Parasites

Front 1

Cause of Babesiosis

Back 1

Babesia microti

Front 2

Transmission of Babesia

Back 2

Deer tics

Front 3

Those at risk for severe infection

Back 3

Immunocompromised
Asplenic
Elderly

Front 4

Presentation of babesiosis

Back 4

Hemolytic anemia w/fever, weakness, jaundice, and hepatosplenomegaly

Front 5

Treatment for Babesiosis

Back 5

Clindamycin and quinine sulfate

Front 6

African Sleeping Sickness

Back 6

Trypanosome brucei gambiense
T. brucei rhodesiense

Front 7

Transmission of sleeping sickness

Back 7

Tsetse fly
(and sexually according to Dr. House)

Front 8

Where do you find T. gambiense? What animal is it transmited through? Are pentamidine and eflornithine effective?

Back 8

West and Central Africa
Transmitted through pigs
Yes

Front 9

Where do you find T. rhodesiense? What animal is it transmited through? Are pentamidine and eflornithine effective?

Back 9

East Africa
Cows
No

Front 10

Trypanosome invasion occurs where early in the dz? In late dz?

Back 10

Early: Blood and lymph
Late: CNS

Front 11

Course of trypanosome meningoencephalitis

Back 11

Somnolence --> Coma --> Death

Front 12

Treatment for the intital stages of Sleeping sickness

Back 12

Suramin (doesn't cross BBB)

Front 13

What drug is coadministered with suramin in T. gambiense infection

Back 13

Pentamidine

Front 14

Treatment once trypanosome infection has reached the brain?

Back 14

Melarsoprol *extremely toxic, but 80-90% cure rate

Front 15

T gambiense relapse treatment

Back 15

Eflornithine

Front 16

T. rhodesiense relapse treatment

Back 16

Re-administer Melarsoprol

Front 17

Tranmission of T. cruzi

Back 17

Blood sucking triatomid bugs
Blood transfusion
Transplacentally

Front 18

Reservoir hosts for T. cruzi

Back 18

Domestic animals

Front 19

Acute Chagas dz usually affects who?

Back 19

Children

Front 20

Where do trypomastigotes divide into amastigotes?

Back 20

Inside cells

Front 21

What systems are seriously infected by T. cruzi? What is the consequence?

Back 21

Heart
Reticulo-endothelial system
ANS
Can lead to cardiac myopathy and chronic dz of the GI tract

Front 22

Treatment for T. cruzi? Can you use these for acute and chronic dz?

Back 22

Nifurtimox and benznidazole
* Not effective against chronic dz

Front 23

Transmission of Leshmaniasis
3 kinds

Back 23

Sandfly
Visceral (kala azar)
Cutaneous
Mucocutaneous

Front 24

In visceral leshmania, where do the promastigotes transform into amastigotes

Back 24

macrophages and other mononuclear phagocytes --> macrophage rupture

Front 25

Infection of visceral leishmania

Back 25

Intermittent fever, dysfxn of liver, spleen, bone marrown, and lymph nodes
*80% fatal

Front 26

Treatment for leishmania

Back 26

Sodium stibogluconate

Front 27

2nd line agent for mucocutaneous leishmaniasis

Back 27

Amphotericin B

Front 28

2nd line agent for visceral leishmaniasis

Back 28

Pentamidine

Front 29

Drugs used to treat blood and tissue parasites

Back 29

Eflornithine (difluoromethylornithine-DFMO)
Melarsoprol (MEL B)
Nifurtimox
Sodium stibogluconate
Suramin

Front 30

DFMO use

Back 30

late stage trypanosomiasis

Front 31

MOA of DFMO

Back 31

Suicide inhibitor of the enzyme ornithine decarboxylase
*10 fold greater affinity for the parasite enzyme than for the host enzyme

Front 32

PK of DFMO

Back 32

Associated w/disappearance of trypanosomes from the body fluids w/i one day.

Front 33

SE of DFMO

Back 33

Diarrhea
Abdominal pain
Anemia

Front 34

Use of MEL B

Back 34

Organic arsenic, used for meningoencephalitic stages of sleeping sickness

Front 35

MOA of Mel B

Back 35

Arsenics react w/sulfhydrl groups in proteins, inactivating enzymes

Front 36

Admin of Mel B

Back 36

Very toxic!
Give by slow i.v.

Front 37

Side Effects of Mel B

Back 37

Hypertension
Abdominal pain
Vomiting
Proteinuria
Peripheral neuropathy
Rashes
Reactive encephalopathy* most severe

Front 38

Nifurtimox activity

Back 38

Active against the amastigote and extracellular mastigote stages
Not effective in the acute or chronic stages

Front 39

MOA of Nifurtimox

Back 39

Converted to a nitrofuran radical then to a superoxide radical and peroxide
All three forms are toxic

Front 40

PK of Nifurtimox

Back 40

Well absorbed from GI, extensively metabolized

Front 41

SE of Nifurtimox

Back 41

High incidence of CNS disturbances w/transitory convulsive episodes, stiffness, and limb weakness

Front 42

Use of sodium stibogluconate

Back 42

All three forms of Leishmaniasis

Front 43

MOA of SS

Back 43

Prodrug converted to trivalent form which may (-) parasite's phosphofructokinase the rate limiting step in glycolysis

Front 44

SE of SS

Back 44

Highly Toxic!
Muscle pain
Joint stiffness
Nausea
Flattened T wave
Occasionally weakness, liver damage, and bradycardia
Also myocardial damage, renal damage, shock and sudden death

Front 45

Use of Suramin

Back 45

Early infections w/T gambiese and rhodesiense

Combined w/diethylcarbamazine to treat O. volvulus infection

Front 46

MOA of Suramin

Back 46

Selectively endocytosed by parasites

Front 47

Admin of suramin

Back 47

Slow i.v.

Front 48

SE of suramin

Back 48

Shock
Coma
*give small test dose first
Paresthesias
Hyperesthesias
Peripheral neuropthy
Photophobia
Nephrotoxic *proteinuria is frequent

Front 49

Why does suramin hang around in the blood for so long?

Back 49

Tightly bound to plasma proteins