ANTIPROTOZOAL Flashcards
(196 cards)
1
Q
What percentage of the world’s population is affected by amebiasis?
A
About 10%
Amebiasis causes invasive disease in about 50 million people and results in approximately 100,000 deaths annually.
2
Q
Which species of Entamoeba requires treatment for amebiasis?
A
E. histolytica
E. histolytica is the third-leading cause of mortality by parasitic infection.
3
Q
How is amebiasis primarily transmitted?
A
Fecal-oral route
4
Q
What are the major clinical manifestations of E. histolytica infection?
A
- Colitis
- Bloody diarrhea (amebic dysentery)
- Amebic liver abscess
5
Q
What is the cornerstone therapy for amebiasis?
A
Metronidazole or its analogue tinidazole
6
Q
What additional treatment is recommended for patients with amebic colitis or liver abscess?
A
A luminal agent in addition to metronidazole
Luminal agents include paromomycin and iodoquinol.
7
Q
What is the causative agent of giardiasis?
A
Giardia intestinalis
8
Q
Which populations are at higher risk for giardiasis transmission?
A
- Children in day-care centers
- Institutionalized individuals
- Male homosexuals
9
Q
What are the three syndromes associated with Giardia infection?
A
- Asymptomatic carrier state
- Acute self-limited diarrhea
- Chronic diarrhea with malabsorption
10
Q
What is the treatment of choice for giardiasis?
A
Metronidazole
Tinidazole may be superior, and paromomycin is safe for pregnant women.
11
Q
What organism causes trichomoniasis?
A
Trichomonas vaginalis
12
Q
What is the most common nonviral sexually transmitted disease?
A
Trichomoniasis
13
Q
What is the main treatment for trichomoniasis?
A
Metronidazole
14
Q
What is the primary host for Toxoplasma gondii?
A
Cats and other feline species
15
Q
What are common routes of infection for toxoplasmosis in humans?
A
- Ingestion of undercooked meat
- Ingestion of contaminated vegetables
- Direct contact with cat feces
- Transplacental infection
16
Q
What is a common clinical manifestation of congenital toxoplasmosis?
A
Chorioretinitis
17
Q
What is the primary treatment for toxoplasmic encephalitis?
A
Pyrimethamine and sulfadiazine with folinic acid
18
Q
What is the role of spiramycin in toxoplasmosis treatment?
A
Used to treat acute acquired toxoplasmosis in early pregnancy
19
Q
What are the primary pathogens causing cryptosporidiosis?
A
- Cryptosporidium parvum
- Cryptosporidium hominis
20
Q
How are Cryptosporidia transmitted?
A
Direct human-to-human contact or contaminated water supplies
21
Q
What is the treatment for cryptosporidiosis in immunocompetent individuals?
A
Nitazoxanide
22
Q
What is the most effective therapy for cryptosporidiosis in immunocompromised patients?
A
Restoration of immune function
23
Q
What is trypanosomiasis commonly known as?
A
Sleeping sickness.
24
Q
What organism causes trypanosomiasis?
A
Trypanosoma brucei.
25
How is trypanosomiasis transmitted?
By bloodsucking tsetse flies of the genus Glossina.
26
In which geographical area is trypanosomiasis primarily found?
Sub-Saharan Africa.
27
What are the two types of African trypanosomiasis?
* East African (Rhodesian; T. brucei rhodesiense)
* West African (Gambian; T. brucei gambiense)
28
What symptoms characterize early-stage trypanosomiasis?
* Febrile illness
* Lymphadenopathy
* Splenomegaly
* Occasional myocarditis
29
What is the standard therapy for early-stage T. brucei gambiense?
Pentamidine.
30
What is the standard therapy for early-stage T. brucei rhodesiense?
Suramin.
31
What is the treatment for late-stage trypanosomiasis?
Eflornithine.
32
What is NECT?
Nifurtimox-eflornithine combination therapy.
33
True or False: Eflornithine is effective against late-stage T. brucei rhodesiense.
False.
34
What is the estimated global prevalence of Chagas disease?
About 6-7 million.
35
What is the primary vector for Chagas disease?
Bloodsucking triatomid bugs.
36
What are the two drugs used to treat Chagas disease?
* Nifurtimox
* Benznidazole
37
What are the major complications of chronic Chagas disease?
* Cardiomyopathy
* Megaesophagus
* Megacolon
* Death
38
What type of disease is leishmaniasis?
Vector-borne zoonosis.
39
What is the primary reservoir for Leishmania?
Small mammals and canines.
40
What are the major syndromes of human leishmaniasis?
* Cutaneous
* Mucocutaneous
* Diffuse cutaneous
* Visceral (kala azar)
41
What is the main treatment for visceral leishmaniasis?
Liposomal amphotericin B.
42
What is the first orally active agent approved for leishmaniasis?
Miltefosine.
43
What is a significant limitation of miltefosine?
Its teratogenic effects limit its use in women of childbearing age.
44
Fill in the blank: The classic therapy for all species of Leishmania is with _______.
Pentavalent antimony compounds.
45
What is the geographical distribution of Chagas disease?
Primarily confined to Latin America.
46
True or False: Chagas disease can be transmitted by blood transfusion.
True.
47
What is Babesiosis?
A tick-borne zoonosis caused by Babesia microti or B. divergens that resembles malaria.
48
What are the symptoms of Babesiosis?
Febrile illness, hemolysis, and hemoglobinuria.
49
In which individuals can Babesiosis be severe or fatal?
In asplenic or severely immunocompromised individuals.
50
What is the therapy for severe Babesiosis?
Combination of clindamycin and quinine.
51
What therapy is used for mild or moderate Babesiosis?
Combination of azithromycin and atovaquone.
52
What is Balantidiasis?
An infection of the large intestine caused by Balantidium coli.
53
How does Balantidiasis differ from amebiasis?
Balantidiasis usually responds to tetracycline therapy.
54
What does Cyclospora cayetanensis cause in normal hosts?
Self-limited diarrhea.
55
What can Cyclospora cayetanensis cause in immunocompromised individuals?
Prolonged diarrhea.
56
What does Cystoisospora belli cause in patients with AIDS?
Diarrhea.
57
What is the treatment for Cyclospora and Cystoisospora infections?
Trimethoprim-sulfamethoxazole.
58
What are Microsporidia classified as?
Fungi.
59
What type of organisms are Microsporidia?
Spore-forming, unicellular, eukaryotic organisms.
60
What is Amphotericin B primarily used for?
Amphotericin B is a highly effective antileishmanial agent that cures >90% of cases of visceral leishmaniasis.
61
What types of leishmaniasis can Amphotericin B treat?
Amphotericin B is used for visceral, cutaneous, and mucosal leishmaniasis.
62
How does the lipid preparation of Amphotericin B affect its toxicity?
Lipid preparations of Amphotericin B have reduced toxicity.
63
What is Eflornithine's mechanism of action?
Eflornithine is an irreversible catalytic (suicide) inhibitor of ornithine decarboxylase.
64
What is the role of polyamines in trypanosomes?
Polyamines (putrescine, spermidine, and spermine) are required for cell division and normal cell differentiation.
65
What distinguishes the susceptibility of Eflornithine between parasite and human enzymes?
Both enzymes are equally susceptible to inhibition, but the mammalian enzyme is turned over rapidly, while the parasite enzyme is stable.
66
How is Eflornithine administered?
Eflornithine is given by intravenous infusion.
67
What is the half-life of Eflornithine?
The half-life of Eflornithine is 3-4 hours.
68
What is the renal clearance rate of Eflornithine after IV administration?
The renal clearance rate is rapid at 2 mL/min/kg.
69
What is NECT and how does it compare to eflornithine alone?
NECT is a combination therapy that is safer and more efficacious than eflornithine alone for late-stage gambiense sleeping sickness.
70
What are the common adverse reactions associated with Eflornithine?
Adverse reactions include abdominal pain, headache, and reactions at injection sites.
71
What severe reactions can occur with Eflornithine alone?
Severe reactions include fever (6%), seizures (4%), and diarrhea (2%).
72
What is the case fatality rate for Eflornithine compared to melarsoprol?
The case fatality rate for Eflornithine is 0.7%-1.2%, while for melarsoprol it is 4.9%.
73
What are the therapeutic uses of Eflornithine?
Eflornithine is used for late-stage West African trypanosomiasis caused by T. brucei gambiense.
74
What is the dosing regimen for treating visceral leishmaniasis with Amphotericin B?
3 mg/kg intravenously on days 1-5, 14, and 21 for a total dose of 21 mg/kg.
75
What is the cure rate for Eflornithine when combined with nifurtimox (NECT)?
NECT achieves a higher cure rate of 96.5% compared to eflornithine alone at 91.5%.
76
Fill in the blank: Amphotericin B complexes with _______ in the cell membrane.
ergosterol precursors
77
True or False: Eflornithine binds to plasma proteins.
False
78
What is the primary biochemical effect of Eflornithine on trypanosomes?
Polyamine depletion.
79
What is melarsoprol used to treat?
Late (CNS) stages of East African trypanosomiasis caused by T. brucei rhodesiense
## Footnote
It is the only drug for this condition despite its risks.
80
What is the first-line treatment for late-stage West African trypanosomiasis caused by T. brucei gambiense?
NECT
## Footnote
Melarsoprol is effective but NECT has become the preferred treatment.
81
Which two halogenated 8-hydroxyquinolines are used as luminal agents?
* Iodoquinol (diiodohydroxyquin)
* Clioquinol (iodochlorhydroxyquin)
## Footnote
They are used to eliminate intestinal colonization with E. histolytica.
82
What is the preferred luminal agent for amebiasis due to its superior adverse-event profile?
Paromomycin
## Footnote
It is preferred over iodoquinol and clioquinol.
83
What is the most important toxic reaction associated with clioquinol?
Subacute myelo-optic neuropathy
## Footnote
This is a serious side effect primarily linked to clioquinol.
84
What is the recommended dose of iodoquinol for adults?
650 mg orally three times daily for 20 days
## Footnote
For children, it is 30-40 mg/kg body weight orally, divided three times a day.
85
What is the mechanism of action of melarsoprol?
Melarsoprol is metabolized to melarsen oxide, which inactivates many enzymes by reacting with vicinal sulfhydryl groups
## Footnote
It specifically binds to trypanothione, inhibiting trypanothione reductase.
86
What is a major risk factor for developing encephalopathy when using melarsoprol?
High parasitemia
## Footnote
A febrile reaction often occurs soon after drug injection, especially if parasitemia is high.
87
What is the dosing regimen for melarsoprol for both T. brucei gambiense and T. brucei rhodesiense?
2.2 mg/kg/d IV for 10 days
## Footnote
This dosing is critical for effective treatment.
88
True or False: Melarsoprol can be administered outside of hospital supervision.
False
## Footnote
It should only be given under hospital supervision due to significant toxicity.
89
What adverse effect can occur in patients treated with melarsoprol after a febrile episode?
Increased incidence of reactive encephalopathy
## Footnote
Initiating therapy during a febrile episode raises the risk of this serious complication.
90
What is the active metabolite of melarsoprol?
Melarsen oxide
## Footnote
It is the form that exerts the therapeutic effect.
91
What is a common side effect of iodoquinol in children with chronic diarrhea?
Optic atrophy and permanent vision loss
## Footnote
This is associated with high doses of iodoquinol.
92
What is the half-life of the active metabolite of melarsoprol?
43 hours
## Footnote
This contributes to the drug's prolonged action.
93
Fill in the blank: Melarsoprol is always administered by _______.
slow intravenous injection
## Footnote
Care must be taken to avoid leakage into surrounding tissues.
94
What should be monitored during melarsoprol treatment due to potential toxicity?
Renal and hepatic function
## Footnote
Albuminuria and other signs of renal or hepatic impairment are common.
95
What is the mechanism of action of metronidazole?
Active against anaerobic protozoal parasites and anaerobic bacteria
## Footnote
Metronidazole is a prodrug requiring reductive activation by susceptible organisms.
96
Which organisms are clinically effective against metronidazole?
* Trichomoniasis
* Amebiasis
* Giardiasis
## Footnote
Other 5-nitroimidazoles include tinidazole, secnidazole, and ornidazole.
97
What types of bacteria does metronidazole exhibit antibacterial activity against?
* Anaerobic cocci
* Anaerobic gram-negative bacilli (e.g., Bacteroides spp.)
* Anaerobic spore-forming gram-positive bacilli (e.g., Clostridium)
* Microaerophilic bacteria (e.g., Helicobacter, Campylobacter)
## Footnote
Nonsporulating gram-positive bacilli are often resistant.
98
How does metronidazole get activated in anaerobic organisms?
Through reductive activation of the nitro group by electron transport components
## Footnote
This process forms a highly reactive nitro radical anion that kills susceptible organisms.
99
What is the preferred treatment regimen for trichomoniasis using metronidazole?
2 g metronidazole as a single oral dose for both males and females
## Footnote
Treatment failures due to metronidazole-resistant strains are becoming more common.
100
What is the recommended dose of metronidazole for amebiasis?
500-750 mg taken orally three times daily for 7-10 days
## Footnote
For children, 35-50 mg/kg/d in three divided doses for 7-10 days.
101
What is the first-line therapy for giardiasis?
Tinidazole as a single 2-g dose
## Footnote
This is an appropriate first-line therapy.
102
What is a common side effect of metronidazole?
* Headache
* Nausea
* Dry mouth
* Metallic taste
## Footnote
Other side effects include vomiting, diarrhea, and abdominal distress.
103
True or False: Metronidazole can cause a disulfiram-like effect when alcohol is consumed.
True
## Footnote
This may result in abdominal distress, vomiting, flushing, or headache.
104
What is the effect of increasing levels of oxygen on metronidazole's activity?
Inhibits metronidazole-induced cytotoxicity
## Footnote
Oxygen competes with metronidazole for electrons, decreasing its activation.
105
Fill in the blank: Metronidazole penetrates well into body tissues and fluids, including _______.
Vaginal secretions, seminal fluid, saliva, breast milk, and CSF
## Footnote
It is distributed to a volume approximating total body water.
106
What are the principal metabolites of metronidazole?
* Hydroxy metabolite (longer t1/2 ~12 h)
* Glucuronides
## Footnote
The hydroxy metabolite has about 50% of the antitrichomonal activity of metronidazole.
107
What should be done if a patient experiences numbness or paresthesias while on metronidazole?
Withdraw metronidazole
## Footnote
Reversal of serious sensory neuropathies may be slow or incomplete.
108
What are some drug interactions associated with metronidazole?
* Disulfiram (confusional states)
* Warfarin (prolonged prothrombin time)
* Lithium (CNS toxicity)
## Footnote
Metronidazole should not be used with disulfiram or any disulfiram-like drug.
109
What is the elimination route for metronidazole after oral dosing?
More than 75% is eliminated in the urine
## Footnote
Mostly as metabolites formed by the liver.
110
What conditions contraindicate the use of metronidazole?
Active disease of the CNS, severe hepatic disease, and first trimester of pregnancy
## Footnote
Caution is advised due to potential neurotoxicity.
111
What type of compound is miltefosine?
An alkylphosphocholine analogue
## Footnote
Developed originally as an anticancer agent.
112
What diseases is miltefosine highly curative against?
Visceral leishmaniasis and cutaneous forms of the disease.
113
What is a major drawback of using miltefosine?
Its teratogenicity; must not be used in pregnant women.
114
What is significant about miltefosine regarding leishmaniasis treatment?
It is the first orally available therapy for leishmaniasis.
115
Is the mechanism of action of miltefosine understood?
No, it is not understood.
116
What may miltefosine alter in its mechanism of action?
Ether-lipid metabolism, cell signaling, or glycosylphosphatidylinositol anchor biosynthesis.
117
What type of transporter is involved in miltefosine's action?
A P-type ATPase belonging to the aminophospholipid translocase subfamily.
118
What leads to drug resistance in miltefosine?
A point mutation in the transporter that leads to decreased drug uptake.
119
What are the two main drugs used to treat American trypanosomiasis?
Nifurtimox and benznidazole.
120
What forms of T. cruzi do nifurtimox and benznidazole target?
Both the trypomastigote and amastigote forms.
121
What is the activation mechanism for nifurtimox and benznidazole?
Activation by an NADH-dependent mitochondrial nitroreductase to nitro radical anions.
122
What cellular damage is caused by the nitro anion radicals from nifurtimox and benznidazole?
Lipid peroxidation, membrane injury, and enzyme inactivation.
123
What leads to drug resistance in nifurtimox and benznidazole?
Reduced nitroreductase expression.
124
What are common side effects of nifurtimox and benznidazole?
Hypersensitivity reactions, nausea, vomiting, myalgia, and weakness.
125
What is the most common adverse event for benznidazole?
Urticarial dermatitis.
126
What should be monitored during benznidazole therapy?
Blood cell counts.
127
What is the recommended dose of miltefosine for adults over 45 kg?
150 mg/kg/d for 28 days.
128
What is the recommended dose of miltefosine for patients weighing 30-45 kg?
100 mg/kg/d.
129
What is the half-life of nifurtimox?
3 hours.
130
What is the half-life of benznidazole?
12 hours.
131
What is the therapeutic range for benznidazole in adults?
3-6 mg/L.
132
What should be avoided during treatment with nifurtimox?
Ingestion of alcohol.
133
What is the recommended treatment duration for nifurtimox in acute infection?
90 days.
134
What is the recommended treatment duration for benznidazole?
60 days.
135
What is the recommended dose of benznidazole for adults?
5-7 mg/kg/d in two divided doses.
136
What should be done if gastric upset occurs during benznidazole treatment?
Adjust the dosage.
137
What is Nitazoxanide?
An oral synthetic broad-spectrum antiparasitic agent
## Footnote
Used for the treatment of cryptosporidiosis and giardiasis in adults and immunocompetent children.
138
What is the active metabolite of Nitazoxanide?
Tizoxanide (desacetyl-nitazoxanide)
## Footnote
It is responsible for the antimicrobial effects of Nitazoxanide.
139
Which parasites does Nitazoxanide inhibit the growth of?
* C. parvum (sporozoites and oocytes)
* G. intestinalis (trophozoites)
* E. histolytica (trophozoites)
* T. vaginalis (trophozoites)
* Intestinal helminthes
## Footnote
It has a broad spectrum of activity against various parasitic infections.
140
What happens to Nitazoxanide after oral administration?
It is rapidly hydrolyzed to tizoxanide, which undergoes conjugation to tizoxanide glucuronide
## Footnote
Maximum plasma concentrations occur 1-4 hours after administration.
141
How is Tizoxanide primarily excreted?
* Urine
* Bile
* Feces
## Footnote
Tizoxanide is more than 99.9% bound to plasma proteins.
142
What is the mechanism of action of Nitazoxanide?
Interferes with the PFOR enzyme-dependent electron-transfer reaction
## Footnote
This reaction is essential to anaerobic metabolism in protozoan and bacterial species.
143
What is the therapeutic efficacy of Nitazoxanide for G. intestinalis infection?
85%-90%
## Footnote
It is also effective for treating diarrhea caused by Cryptosporidia (56%-88%).
144
What is the recommended dose of Nitazoxanide for children ages 12-47 months to treat cryptosporidiosis?
100 mg every 12 hours for 3 days
## Footnote
For children ages 4-11 years, the dose is 200 mg every 12 hours for 3 days.
145
What are the side effects of Nitazoxanide?
Rare adverse effects, including a greenish tint to urine
## Footnote
Nitazoxanide is classified as a pregnancy category B agent.
146
What is Paromomycin?
An aminoglycoside used to treat E. histolytica infection, cryptosporidiosis, and giardiasis
## Footnote
It is part of the neomycin/kanamycin family.
147
What is the mechanism of action of Paromomycin?
Binds to the 30S ribosomal subunit
## Footnote
It shares this mechanism with neomycin and kanamycin.
148
What is the drug of choice for treating intestinal colonization with E. histolytica?
Paromomycin
## Footnote
It is used in combination with metronidazole to treat amebic colitis.
149
What are the common adverse effects associated with Paromomycin?
* Abdominal pain
* Cramping
* Nausea
* Vomiting
* Steatorrhea
* Diarrhea
## Footnote
Rarely, rash and headache may occur.
150
What is the dosing recommendation for Paromomycin?
25-35 mg/kg/day in three divided oral doses
## Footnote
This applies to both adults and children.
151
Fill in the blank: Paromomycin is used in pregnant women and for _______ resistant isolates.
metronidazole
## Footnote
It is an effective alternative when metronidazole is not suitable.
152
What is pentamidine?
A positively charged aromatic diamine used as a broad-spectrum agent against several pathogenic protozoa and some fungi.
153
What form is pentamidine marketed in?
As the di-isethionate salt for injection or as an aerosol.
154
Which infection is pentamidine used to treat?
Early-stage T. brucei gambiense infection.
155
Is pentamidine effective for late-stage T. brucei infections?
No, it is ineffective in the treatment of late-stage disease.
156
What is an alternative agent for cutaneous leishmaniasis?
Pentamidine.
157
What pneumonia does pentamidine prophylaxis target?
Pneumonia caused by Pneumocystis jiroveci (PJP).
158
What is a less expensive alternative to pentamidine for early African trypanosomiasis?
Diminazene.
159
What is known about the mechanism of action of diamidines like pentamidine?
The mechanism of action is unknown.
160
Which transporter is responsible for pentamidine uptake?
TbAQP2 from the aquaglyceroporin gene family.
161
What is the half-life of pentamidine after intravenous administration?
Several minutes to a few hours.
162
What percentage of pentamidine is bound to plasma proteins?
70%.
163
Is pentamidine well absorbed orally?
No, it is poorly absorbed orally.
164
What is the treatment dosage for early-stage T. brucei gambiense using pentamidine?
4 mg/kg daily for 7 days.
165
What are the typical doses for treating cutaneous leishmaniasis with pentamidine?
2-3 mg/kg IV or IM daily or every second day for 4-7 doses.
166
What percentage of individuals show adverse effects from pentamidine?
50%.
167
What are some adverse effects associated with intravenous pentamidine administration?
Hypotension, tachycardia, headache.
168
What life-threatening condition may occur during pentamidine treatment?
Hypoglycemia.
169
What renal side effect is associated with pentamidine?
Nephrotoxicity, with ~25% showing signs of renal dysfunction.
170
What is sodium stibogluconate used for?
Treatment of leishmaniasis and other protozoal infections.
171
What type of compound is sodium stibogluconate?
A pentavalent antimonial compound.
172
How do pentavalent antimonials like sodium stibogluconate work?
They act as prodrugs that are reduced to the more toxic Sb3+ species.
173
What is the standard dosage for sodium stibogluconate in treating cutaneous leishmaniasis?
20 mg/kg/d for 20 days.
174
What are some common adverse effects of sodium stibogluconate?
Chemical pancreatitis, elevation of serum hepatic transaminases, bone marrow suppression.
175
True or False: Most toxic reactions from sodium stibogluconate are irreversible.
False.
176
What is the elimination route for sodium stibogluconate?
In the urine.
177
What is suramin primarily used for?
Treatment of African trypanosomiasis
## Footnote
Suramin has no clinical utility against American trypanosomiasis.
178
When was suramin introduced into therapy?
1920
## Footnote
This followed research into the trypanocidal activity of certain dyes.
179
What is the mechanism of action of suramin?
Unknown
## Footnote
A recent study suggested a role for lysosomal function and ISG75 family mediating suramin uptake.
180
Why is suramin administered intravenously?
It is not absorbed after oral intake
## Footnote
This avoids local inflammation and necrosis associated with subcutaneous or intramuscular injections.
181
What is the terminal elimination half-life (t1/2) of suramin?
41-78 days
182
What percentage of suramin is bound to serum protein?
99.7%
183
What accounts for 80% of suramin's elimination from the body?
Renal clearance
184
What is the first-line therapy for early-stage T. brucei rhodesiense infection?
Suramin
185
What should be ensured before starting treatment for active African trypanosomiasis?
No CNS involvement
## Footnote
Treatment should not start until 24 hours after diagnostic lumbar puncture.
186
What is the normal single dose of suramin for adults with T. brucei rhodesiense infection?
1 g
187
What is the advised test dose of suramin for adults?
100 mg
188
What serious immediate reactions can occur with suramin?
Nausea, vomiting, shock, loss of consciousness
189
What is a potential reaction in individuals with onchocerciasis when treated with suramin?
Mazzotti reaction
## Footnote
Symptoms include pruritic rash, fever, malaise, lymph node swelling, eosinophilia, arthralgias, tachycardia, hypotension, and possibly permanent blindness.
190
What is the pediatric test dose of suramin?
2 mg/kg
191
What should be done for patients who relapse after suramin therapy?
Treat with melarsoprol
192
Suramin is known to inhibit many ______ and receptors.
trypanosomal enzymes
193
True or False: Suramin is effective for late-stage African trypanosomiasis.
False
## Footnote
Very little suramin penetrates the CSF.
194
What kind of activity does suramin exhibit against T. brucei gambiense?
High clinical activity
195
What kind of pharmacokinetics does suramin display?
Complex pharmacokinetics with marked interindividual variability
196
What type of solutions should be used for suramin?
Freshly prepared solutions
## Footnote
Solutions deteriorate quickly in air.
