Covers required drugs for lectures 61 and 62 antiparasitics 1&2
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| Iodoquinol* is used to treat what | E. histolytica, only useful in treatment of intestinal amebiasis
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| Mechanism of action of Iodoquinol* | liberates iodine which is the active amebicide
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| What is the pharmacology of Iodoquinol* | not readily absorbed from GI tract so it is effective in treating intestinal infections
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| Side effects of Iodoquinol* | Low dose: headache, diarrhea, nausea, vomiting, skin rashes, anal puritis, and slight thyroid enlargement in some. High dose: causes loss of visual acuity, optical atrophy and blindness
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| What is Paromomycin* used to treat | useflul only in the treatment of intestinal amebiasis and some intestinal cestode infections
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| What is the mechanism of action of Paromomycin* | It acts on protein synthesis by binding to the 16S ribosomal RNA of the 30S ribosomal subunit, it is an aminoglycoside antibiotic
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| What is the pharmacology of Paromomycin* | Poorly absorbed from the intestine.
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| What are the side effects of Paromomycin* | Main side effects are diarrhea and abdominal pain, and sometimes nausea or dizziness. It can also alter bowel bacteral population and a GI superinfection can be a problem.
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| Drugs used to treat asymptomatic or mild intestinal only amebiasis | Iodoquinol*, Paromomycin*
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| Drugs used to treat Mixed amebicides | Metronidazole* for the systemic infection, with Diloxanide furoate or Iodoquinol* to treat the intestinal infection.
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| What is used to treat Cryptosporidium: a water-borne coccidian protozoan that causes diarrhea | Nitazoxanide* is about 80% effective and is approved for treatment of children over 12 months.
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| What is used to treat Cyclospora cayetanensis: causes diarrhea in AIDS patients | Trimethoprim-sulfamethoxazole (TMP/SMX)*
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| What is used to treat Giardia lamblia: cause of traveler's diarrhea from water contamination | Metronidazole*, 85-90% effective (Not FDA apporved). Nitazoxanide* is available in a pediatric liquid suspension. Paromomycin* should be used to treat pregnant women.
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| What is used to treat Isospora belli: tropical cause of diarrhea | Trimethoprim-sulfamethoxazole (TMP/SMX)*
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| What is used to treat Trichomonas vaginalis: The common pathogen of the urogenital tract | Metronidazole*. periodic vinegar douches in women can restore the protective acidic environment of the vagina (T vaginalis can't survive a pH below 4.9)
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| Metronidazole* is used to treat what | E. histolytica, T. vaginalis, G. lamblia, and anaerobic bacteria such as Clostridia and Bactreoides
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| What is the mechanism of action of Metronidazole* | It acts as electron sink to prevent the terminal electron transport system from re-oxidizing NADH and NADPH in anaerobic and microaeorophilic organisms. Once reduced Metronidazole is toxic and can introduce DNA strand modifications
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| What is the pharmacology of Metronidazole* | well absorbed by the GI tract, extensively metabolized (metabolite are mutagenic), eliminated by the kidneys
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| What are the side effects of Metronidazole* | GI upset, metallic taste. DISULFIRAM-like effect if taken within 24 hrs of EtOH consumption. Rarely,nervous system toxicities: weakness, paresthesias, vertigo, and ataxia. Avoid in pregnancy carcinogenic/teratogenic in animals mutagenic in bacteria
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| What is Nitazoxanide* used to treat | FDA approved to treat giardiasis and cryptosporidiosis in kids over 1. May be effective against other intestinal parasites including helminths. Good for Metronidazole resistant organism because it has a different mechanism
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| What is the mechanism of action of Nitazoxanide* | Inhibits parasties' pyruvate-ferredoxin oxidoreductase, which is essential in anaerobic energy metabolism.
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| What is the pharmacology of Nitazoxanide* | it is given in 3 oral doses, absorbed for GI tract and 1/3 of oral dose excreted in urine, 2/3 in feces. the active species is its metabolite tizoxanide which is liberated by hydrolysis in blood.
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| What is Tizoxanide | The active metabolite of Nitazoxanide* liberated by hydrolysis in the blood
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| What are the side effects of Nitazoxanide* | Very mild, not significantly different from placebo. No known drug interactions. Safety in pregnant or lactating women not proven.
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| What are the common diseases in AIDS patients | cryptosporidiosis, cyclosporiasis, isosporiasis, microsporidiosis, pneumocystis, toxoplasmosis
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| What is the treatment of choice for toxoplasmosis infections: can cause encephalitiis especially in HIV patients | Pyrimethamine* with sulfadizine*. (leucovorin to prevent pyrimethamine induced bone marrow suppression). Pregnant women should not take pyrimethamine*.
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| All patients on pyrimethamine* treatment must also take this | Leucovorin a folinic acid supplement to prevent bone marrow suppression.
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| What prophylactic treatment can be given for toxoplasma seropositive HIV patients with low CD4 counts | TMP/SMX* or Pyrimethamine*+Dapsone+Leucovorin.
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| What is the treatment for Pneumocystis jiroveci (PCP): which presents as a respiratory illness in immunocompromised individuals | TMP/SMX*, AIDS paitents have high rates of adverse reactions to this. Pentamidine isethionate* is a second line choice for those intolerant of TMP/SMZ* and have a mild illness.
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| What is the Prophylactic treatment of PCP | TMP/SMX* or inhalation of aerosolized Pentamidnie*
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| What is the mechanism of action of pyrimethamine* | Folate antagonist: blocks reduction of Dihydrofolic acid to Tetrahydrofolic acid
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| What is Atovaquone used to treat | Second line treatment of PCP, toxoplasmosis, and babesiosis. Also used for microsporidiasis in AIDS patients.
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| What is the mechanism of Atovaquone | An inhibitory analog of ubiquinone which interferes with mitochondrial electron transport and related processes
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| What is the pharmacology of Atovaquone | Not well absorbed so it is given with fat to aid absorptions. Half life is 2-3days. It isn't metabolize and is excreted unchanged. 99% is bound to plasma proteins.
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| What are the side effects of Atovaquone | Few which include: rash, fever, vomiting, and headache
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| What are 3 drugs that interfere with Folate and where do they act | Sulfonamides: Block the conversion of Pteridine*+PABA to dihydropteric acid, a precursor of dihydrofolic acid. Trimethoprim and Pyrimethamine* block the reduction of dihydrofolic acid to tetrahydrofolic acid
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| What are the sources of Folate | Food-> Folic acid-> Dihydrofolic acid-> Tetrahydrofolic acid. or Pteridine+PABA-> Dihydropteric acid-> Dihydrofolic acid-> Tetrahydrofolic acid
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| What is Pentamidine Isethionate* used to treat | Trypanosomiasis gambiense, Leishmania donovani (kala azar), Pneumocystis jiroveci
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| What is the mechanism of Pentamidine Isethionate* | Causes selective breaks in the kinetoplast mini-circle DNA of trypanosomes which disrupts DNA replication
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| What is the pharmacology of Pentamidine Isethionate* | Given i.m. or i.v., NOT well absorbed from the gut. Stored in tissues and excreted unchanged
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| What are the side effects of Pentamidine Isethionate* | Immediate effects: hypotension, tachycardia, dizziness, fainting, headaches and vomiting. Reversible renal and hepatic damage seen. Also, selectively toxic to pancreatic beta cells, causing insulin release and hypoglycemia, and eventually irreversible DM
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| What is the treatment for Babesia microti: transmitted by deer tick presents as hemolytic anemia with fever, weakness, jaundice, and hepatosplenomegaly | clindamycin and quinine
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| What is the treatment of African Trypanosomiasis (sleeping sickness): transmitted by tsetse fly | T. brucei gambiense(W. Africa): inital stage Pentamidine*, late stage Melarsoprol or Eflorinithine*. T. brucei rhodesiense(E. Africa): initial stage Suramin, late stage Melarsoprol
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| What is the treatment of choice for Trypanosomiasis meningoencephalitis | Melarsoprol because it crosses the blood brain barrier (But it is extreamly toxic so don't use if CNS uninfected)
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| What is the treatment of American Trypanosomiasis (Chagas Disease) caused by T. Cruzi: transmitted by blood-sucking triatomid bugs and causing cardiac myopathy and chronic GI disease | Nifurtimox and Benznidazole are used to treat acute infection and prevent chronic disease, but neither drug is effective against chronic infection.
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| What is the treatment of Leishmaniais: transmitted by the sandfly causing either visceral leishmaniasis, cutaneous leishmaaniasis, or mucocutaneous leishmaniasis | In the US Sodium Stibogluconate is the first line choice. Amphotericin B is a good second line drug for mucocutaneous or visceral leishmaniasis. Pentamidine* is a good second line choice for visceral leishmaniasis resistant to antimony.
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| What is Eflornithine* used to treat | Late stage trypanosomiasis
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| What is the mechanism of Eflornithine* | Suicide inhibitor of ornithine decarboxylase(key enzyme of polyamine biosynthesis and a requisite for DNA synthesis and cell replication). It has a 10 fold greater affinity for the parasite enzyme than for the host enzyme
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| What is the pharmacology of Eflornithine* | associated with the disappearance of trypanosomes from body fluids, sometimes within one day
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| What are the side effects of Eflornithine* | Generally well-tolerated but can cause diarrhea, abdominal pain, and anemia.
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| What is Melarsoprol used for | Used only for the meningoencephalitic stages of sleeping sickness becuase of toxicity and because it's class is the only one that can cross the blood brain barrier
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| What is the mechanism of Melarsoprol | reacts with sulfhydryl groups in proteins, inactivating a wide variety of enzymes
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| What is the the pharmacology of Melarsoprol | Given by slow i.v injection and very irritating
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| What are the side effects of Melarsoprol | Very toxic: hypertension, abdominal pain, vomiting, proteinuria, peripheral neuropathy, rashes. The most serious, common and potentially fatal side effect is reactive encephalopathy.
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| What is Nifurtimox used for | Active against the amastigote and the extracellular mastigote stages of T. Cruzi
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| What is the mechanism of Nifurtimox | converted to nitrofuran radical and then to a superoxide radical and a peroxide. All 3 forms toxic to the parasite
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| What is the pharmacology of Nifurtimox | Well absorbed from the GI and extensively metabolized
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| What are the side effects of Nifurtimox | High incidence: CNS disturbances with transitory convulsive episodes, stiffness, and weakness in the limbs
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| What is Sodium Stibogluconate used for | Treatment of all three forms of Leishmaniasis
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| What is the mechanism of Sodium Stibogluconate | It is a prodrug which is converted to a trivalent form that may inhibit the parasite's phosphofructokinase, the rate-limiting step in glycolysis
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| What are the side effects of Sodium Stibogluconate | Highly toxic. Common adverse side effects: muscle pain, joint stiffness, nausea,flattend T wave. Occasional: weakness, liver damage and radycardia. Also: myocardial and renal damage, shock or sudden death
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| What is Suramin used for | Treats early infections of T. gambiese and rhodesiense. Can be combined with Diethylcarbamazine to treat O. volvulus infection
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| What is the mechanism of Suramin | Doesn't diffuse across mammalian cell membranes, selectively endocytosed by parasites. Inhibits large numbers of enzymes, specific target unknown
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| What is the pharmacology of Suramin | Administered by slow i.v. binds tightly to serum proteins which cause it to remain in circulation for prolonged periods. Small test doses administered first
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| What are the side effects of Suramin | Serious idiosyncratic reaction possible: shock, coma (small test doses given first). Also causes nervous system disorders: paresthesias, hyperesthesias, peripheral neuropathy, and photophobia. Nephrotoxic resulting in proteinuria
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