Document Details

Uploaded by Deleted User

Southwestern University

Tags

antiprotozoal drugs medicine parasitology disease treatment

Summary

This document covers different antiprotozoal drugs and their mechanisms of action, along with details on malaria. It includes characteristics of protozoal infections and their treatments, along with a crossword puzzle to help with memorization. The study guide also includes explanations on important protozoal infections.

Full Transcript

LAS #9 ANTIPROTOZOAL DRUGS Group 9 SOUTHWESTERN UNIVERSITY PHINMA BSPHA YEAR 3-1 Protozoal Infections Protozoal disease are highly prevalent in tropical third world countries. This is due to the poor sanitary...

LAS #9 ANTIPROTOZOAL DRUGS Group 9 SOUTHWESTERN UNIVERSITY PHINMA BSPHA YEAR 3-1 Protozoal Infections Protozoal disease are highly prevalent in tropical third world countries. This is due to the poor sanitary conditions, hygienic practices, and the control of Vectors of transmission are inadequate. Protozoa Characteristics 05 Divide by binary fission, 01 Unicellular eukaryotic microorganism schizogony, or budding GROUP 9 BSPHA C1 02 Free-living or parasitic 06 Microscopic and complex internal structure 03 Lack cell wall 04 Generally heterotrophic GROUP 9 BSPHA C1 Protozoal Infections Protozoal cells have metabolic processes closer to the human host than to prokaryotic bacterial pathogens. Which makes protozoal diseases less easily treated than bacterial infections. Antiprotozoal drugs cause serious toxic effects to host particularly on cells showing high metabolic activity. Most antiprotozoal agents havenot proven to be safe for pregnantpatients. GROUP 9 BSPHA C1 SWU MALARIA Malaria is an acute infectious disease caused by a few species of the protozoal genus Plasmodium. It is transmitted to humans through the bite of a female Anopheles mosquito. SWU MALARIA Why does the malarial parasite carried only by female Anopheles mosquitoes and not by male Anopheles mosquitoes? SWU MALARIA Male mosquitoes feed only on plant juices, such as nectar to get the sugar they need for energy and survival. As males do not bite, they cannot transmit diseases. On the other hand, female Anopheles mosquitoes need blood proteins to produce eggs. To obtain blood, females seek out and bite hosts such as humans and may transmit disease in the process. SWU MALARIA Species of plasmodium that cause human malaria: Plasmodium falciparum- the most dangerous species responsible for the majority of severe complications and deaths. Plasmodium vivax- causes a milder form of the disease. Plasmodium malariae- common to many topical regions. Plasmodium ovale- rarely encountered. Plasmodium knowlesi- is primarily a pathogen of monkeys but has recently been recognized to cause illness, including severe disease in humans in Southeast Asia. SWU LIFE CYCLE OF THE PARASITE GAMETOCYTES ARE BEING TAKEN UP AB A AN INFECTED FEMALE 9 FEMALE ANOPHELES MOSQUITO FROM AN INFECTED HUMAN, WHERE THEY DEVELOP 1 INTO INFECTIVE SPOROZOITES ANOPHELINE MOSQUITO INJECTS SPOROZOITES. SOME MEROZOITES 8 BECOME GAMETOCYTES SPOROZOITES CIRCULATE 2 RAPIDLY TO THE LIVER TO INVADE LIVER CELLS TROPHOZOITE MULTIPLIES, PRODUCING 7 NEW MEROZOITES. THESE ARE RELEASED WHEN THE ERYTHROCYTE RUPTURES AND AFFECTS OTHER ERYTHROCYTES. EXOERYTHROCYTIC STAGE TISSUE: 3 SCHIZONTS (ACTIVE HEPATIC FORM) AND HYPNOZOITES (DORMANT HEPATIC FORM) MATURE IN THE LIVER 6 IN THE ERYTHROCYTE, THE MEROZOITE BECOMES A TROPHOZOITE. SCHIZONT MULTIPLIES INTO 4 THOUSANDS OF OTHER FORMS MEROZOITES ARE RELEASED 5 KNOWN AS MEROZOITES FROM THE LIVER AND INVADE SWU THE ERYTHROCYTE DRUGS CLASSIFICATION Tissue Schizonticides (Primaquine)- drugs that eliminate developing or dormant liver forms. Blood Schizonticides (Artemisinin, Chloroquine) - drugs that act on erythrocytic parasites. Gametocides (Primaquine)- drugs that kill gametocytes and prevent transmission to mosquitos. Sporonticides (Proguanil, Pyrimethamine)- destroy sporozoites. SWU I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities Inhibits the action of heme Prophylaxis and polymerase in malarial treatment in areas trophozoites, preventing the pruritus, nausea, vomiting, abdominal without resistant P. 1. CHLOROQUINE conversion of heme to pain, headache, anorexia, GI upset, falciparum; treatment of hemozoin. Intracellular rash, blurring of vision P vivax and P ovale malari accumulation of heme is toxic to the parasite. Its antimalarial activity 2. ARTEMISININS appears to result from the Standard of care for (ARTESUNATE, production of free radicals treatment of nausea, vomiting, diarrhea, and ARTEMETHER, that follows the iron-catalyzed uncomplicated dizziness DIHYDROARTEMISININ) cleavage of the artemisinin falciparum malaria GROUP 9 BSPHA C1 endoperoxide bridge. gastrointestinal distress, skin rash, Prophylaxis and headache, dizziness, (at high doses) 3. MEFLOQUINE UNKNOWN treatment in areas with cardiac conduction defects, resistant P falciparum psychiatric disorders, and neurologic effects, including seizures. I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities Cinchonism (tinnitus, headache, The main use of quinine nausea, dizziness, flushing, Complexes with double-stranded is in P falciparum visual disturbances, marked DNA prevent strand separation, infections resistant to visual and auditory 4. QUININE resulting in a block of DNA chloroquine in patients abnormalities, vomiting, replication and transcription to who can tolerate oral diarrhea, abdominal pain, G6PD RNA, prevent protein synthesis treatment deficiency, skin rash, blackwater fever Unknown Eradication of liver (forms quinoline-quinoline stages of P vivax and P nausea, epigastric pain, 5. PRIMAQUINE metabolites, which are electron- ovale, alternative abdominal cramps, headache, transferring redox compounds that chemoprophylaxis fro and methemoglobinemia. GROUP 9 BSPHA C1 act as cellular oxidants.) all species I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities -Malaria treatment and - Bone marrow suppression. Inhibits DHFR (Dihydrofolate reductase) prevention - Skin reactions. 6. PYRIMETHAMINE enzyme, disrupting DNA/RNA synthesis - Toxoplasmosis treatment. - Gastrointestinal via folate metabolism inhibition - Combination therapies. disturbances. -Malaria treatment and -Gastrointestinal disturbances. Inhibits DHFR enzyme, impeding prevention - Mouth ulcers. PROGUANIL DNA/RNA synthesis through folate - Rheumatoid arthritis - Megaloblastic anemia metabolism disruption (sometimes) potential - Malaria treatment - Gastrointestinal issues. Targets dihydropteroate synthase, (combined). SULFADOXINE - Skin rash, photosensitivity. hindering folate synthesis - Toxoplasmosis (rarely). GROUP 9 BSPHA C1 - Hypersensitivity reactions. - Combination therapies - Hemolytic anemia - Leprosy treatment. - Methemoglobinemia. - PCP prevention/treatment Inhibits dihydropteroate synthase, - Skin reactions, GI DAPSONE in HIV patients. suppressing folate synthesis. disturbances. - Dermatitis herpetiformis - Peripheral neuropathy (long- treatment. term) I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities - Gastrointestinal disturbances (nausea, - Bacterial infections vomiting, diarrhea). (respiratory, urinary tract, - Photosensitivity. skin, etc.). Binds to 30S ribosomal subunit, - Tooth discoloration - Lyme disease. inhibiting bacterial protein (children, during tooth - Acne treatment. 7. Doxycycline synthesis by preventing amino development). - Malaria prophylaxis (with acid incorporation into growing - Potential bone development GROUP 9 BSPHA C1 other drugs). peptides impact (children). - Certain sexually - Candidiasis (yeast infection) transmitted infections due to flora disruption. (chlamydia, gonorrhea). - Intracranial hypertension (pseudotumor cerebri, rare). I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities -Liver toxicity (rare, but potentially severe). - Hemolytic anemia Inhibits hemozoin formation within - Malaria treatment and (especially in individuals with Plasmodiumparasites, leading to prevention. - Combined 8. Amodiaquine G6PD deficiency). toxic buildup of heme and parasite with other antimalarials - Central nervous system death in various regimens. effects (dizziness, headache). - QT interval prolongation (rare). GROUP 9 BSPHA C1 Atovaquone: Inhibits mitochondrial -Headache. electron transport, disrupting ATP - Abnormal dreams. - Malaria treatment and production in Plasmodium parasites. - Mouth ulcers. 9. Atovaquone-Proguanil prevention (both - Potential for rash. (Malarone) Proguanil: Inhibits DHFR enzyme, uncomplicated and - Rarely, liver function prophylaxis). impeding folate metabolism and DNA abnormalities. synthesis - Allergic reactions (rare). I. Drugs used in the treatment of malaria Drug MoA Uses AE/ Toxicities Gastrointestinal disturbances (nausea, Inhibits heme polymerase vomiting). - Headache, - Malaria treatment (used enzyme, disrupting heme dizziness. - Liver function less commonly due to 10. Halofantrine detoxification in Plasmodium abnormalities (rare). - safety concerns and parasites, leading to Muscle and joint pain. - resistance). parasite death Skin reactions (rash, itching). - Visual GROUP 9 BSPHA C1 disturbances. II. Drugs used for Amebiasis Drug MoA C/U AE/ Toxicities Unknown Mild toxicity (Diloxanide furoate is converted Luminal amebicide Gastrointestinal symptoms (flatulence-common/ nausea and 1. Diloxanide furoate in gut to diloxanide freebase Asympomatic amebiasis vomiting- infrequent) form which is the active Mild intestinal disease Rashes (rare) amebicide) Not recommended in pregnancy Tissue amebicide Balantidial dysentery Inhibit protein synthesis by Fluke infestation (fascioliasis & Cardiac arrythmias blocking ribosomal movement Heart failure along messenger RNA paragonimiasis) Hypotension 2. Emetines (Emetine and GROUP 9 BSPHA C1 Protoplasmic poison that Used in Severe Neuromuscular effects (pain dehydroemetine) inhibit protein synthesis in amebiasis w  hen and weakness) protozoan and mammalian Metronidazole can't be GI distress (nausea and cells by preventing protein used diarrhea) elongation. Administered parenterally (SC-preferred/IM-supervised) II. Drugs used for Amebiasis Drug MoA C/U AE/ Toxicities Diarrhea (stops a few days) Anorexia Nausea and Vomiting Luminal amebicide Abdominal pain Unknown Alternative to diloxanide for Headache but effective against the 3. Iodoquinol Mild-severe intestinal Rash trophozoites of infections Pruritus Entamoeba histolytica Acute & chronic amebiasis Thyroid enlargement (after high doses) Neurotoxic effects (peripheral GROUP 9 BSPHA C1 neuropathy and visual dysfunction) II. Drugs used for Amebiasis Drug MoA C/U AE/ Toxicities DOC in severe intestinal wall disease and in hepatic Metronidazole- Metronidazole undergoes a abscess and other Gastrointestinal reductive bioactivation of its nitro extraintestinal amebic irritation, headache, group by ferredoxin (present in disease. paresthesias, & dark 4. Metronidazole and anaerobic parasites) to form Used with luminal amebicide coloration of urine. Tinidazole reactive cytotoxic products. Metronidazole- DOC for Tinidazole- similar Trichomoniasis. but better tolerated. Tinidazole is assumed to be Tinidazole- may be effective Serious toxicities similar. against metronidazole- (Neutropenia, resistant organisms dizziness, ataxia) Giardiasis (tinidazole) GROUP 9 BSPHA C1 Abdominal distress Luminal amebicide Diarrhea Asymptomatic infection Inhibits protein synthesis by Headaches 5. Paromomycin Cryptosporidiosis in AIDS binding to 16s ribosomal RNA. Dizziness patients Rashes Leishmaniasis Arthralgia II. Drugs used for Amebiasis Drug MoA C/U AE/ Toxicities Against Giardia lamblia and Rapidly absorbed and converted Cryptosporidium parvum to tizoxanide and tizoxanide Metronidazole-resistant Stomach pain conjugates. Active metabolite, protozoal strains Headache 6. Nitazoxanide tizoxanide, inhibits pyruvate- Used against E. histolytica, nausea ferredoxin oxidoreductase H. pylori, Ascaris discolored urine pathway. lumbricoides, and Fasciola hepatica GROUP 9 BSPHA C1 III. Drugs for Pneumocytosis and Toxoplasmosis Drug MoA C/U AE/ Toxicities First choice in Prophylaxis and tx of Pneumocystis pneumonia (PCP) Prophylaxis in AIDS patient Toxicity- A/E occurs in up Prophylactic against to 50% Toxoplasmosis GI distress Inhibits folic acid Infections by Isospora belli 1. TMP-SMZ Rash synthesis UTI Fever Respiratory, ear, and sinus GROUP 9 BSPHA C1 Neutropenia infection by Haemophilus Thrombocytopenia influenzae a nd Moraxella catarrhalis. DOC for Nocardiosis Cholera, typhoid fever and shigellosis (back up drug) III. Drugs for Pneumocytosis and Toxoplasmosis Drug MoA C/U AE/ Toxicities Severe AE follow after parenteral use, particularly respiratory stimulation followed by Depression Primary and secondary Unknown but may involve Hypotension from Prophylaxis of P. jiroveci inhibition of glycolysis or peripheral vasodilation pneumonia 2. Pentamidine interference with nucleic acid Hypoglycemia Active Pneumocytosis in metabolism of protozoans and anemia HIV infected patient fungi Neutropenia African Trypanosomiasis hepatitis GROUP 9 BSPHA C1 pancreatitis Systemic toxicity minimal when used as inhalation III. Drugs for Pneumocytosis and Toxoplasmosis Drug MoA C/U AE/ Toxicities High doses associated with Gastric irritation, glossitis, neurologic Combination has symptoms (headache, synergistic activity against insomnia, tremors, Toxoplasma gondii seizures) and 3. Pyrimethamine + Sequential blockade of 2 steps First line therapy for Acute hematotoxicity Sulfadiazine in folic acid synthesis toxoplasmosis (megaloblastic anemia, Toxoplasma encephalitis in thrombocytopenia) GROUP 9 BSPHA C1 AIDS Antibiotic-associated pseudomembranous colitis may occur during treatment with clindamycin III. Drugs for Pneumocytosis and Toxoplasmosis Drug MoA C/U AE/ Toxicities Common AE (rash, cough, nausea, vomiting, diarrhea, Mild-moderate fever, and abnormal liver pneumocystis pneumonia function test) Inhibit mitochondrial electron Chemoprophylaxis and Avoided in p  atients with 4. Atovaquone transport and folate treatment of chloroquine- history of cardiac metabolism resistant malaria (used in conduction defects, combination with proguanil psychiatric disorder, or (Malarone)) seizures. GROUP 9 BSPHA C1 Not advised for pregnant women IV. Drugs for Trypanosomiasis Drug MoA Uses AE/ Toxicities Severe AE follows after parenteral use, particularly respiratory Used in the hemolymphatic stimulation followed by stages of disease caused depression by Trypanosoma Unknown but may involve hypotension from gambiense and T inhibition of glycolysis or peripheral vasodilation rhodesiense, also known 1. Pentamidine interference with nucleic acid hypoglycemia as African trypanosomiasis GROUP 9 BSPHA C1 metabolism of protozoans and anemia (sleeping sickness). fungi. neutropenia Pneumocytosis hepatitis Treatment of the kala azar pancreatitis form of leishmaniasis Systemic toxicity is minimal when used by inhalation IV. Drugs for Trypanosomiasis Drug MoA Uses AE/ Toxicities AE: Fever, vomiting, abdominal pain, and First-line therapy for arthralgias advanced central nervous The most important system East African Inhibits enzyme sulfhydryl toxicity: reactive 2. Melarsoprol trypanosomiasis groups encephalopathy Second-line therapy for Other serious toxicities: advanced West African renal and cardiac disease trypanosomiasis GROUP 9 BSPHA C1 and hypersensitivity reactions IV. Drugs for Trypanosomiasis Drug MoA Uses AE/ Toxicities Drug of choice in American trypanosomiasis (Chagas disease) Alternative agent in the inhibits the parasite unique Toxicities: allergies, treatment of African 3. Nifurtimox enzymetrypanothione gastrointestinal irritation, trypanosomiasis (Sleeping reductase and CNS effects. sickness) Effective in GROUP 9 BSPHA C1 mucocutaneous leishmaniasis IV. Drugs for Trypanosomiasis Drug MoA Uses AE/ Toxicities Drug of choice for the early hemolymphatic stages of African trypanosomiasis Skin rashes, 4. Suramin Unknown An alternative to ivermectin Gastrointestinal distress, in the treatment of Neurologic complications onchocerciasis (river blindness) GROUP 9 BSPHA C1 IV. Drugs for Trypanosomiasis Drug MoA Uses AE/ Toxicities The only new drug registered to treat African trypanosomiasis (sleeping Gastrointestinal irritation sickness) Inhibitor of ornithine Hematotoxicity 5. Eflornithine First-line drug for decarboxylase Seizures have occurred in advanced West African overdose trypanosomiasis, but is not effective for East African GROUP 9 BSPHA C1 disease V. Drugs for Leishmaniasis Drug MoA Uses AE/ Toxicities Inhibition of glycolysis or First-line agents for AE: GI symptoms, fever, 1. Sodium effects on nucleic acid cutaneous and visceral headache, myalgias, stibogluconate metabolism. leishmaniasis arthralgias, and rash GROUP 9 BSPHA C1 B. Answer the crossword puzzle GROUP 9 BSPHA C1 B. Answer the crossword puzzle 1. This drug is an aminoglycoside that is used for luminal amebecide. GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A R O M O M Y C I N GROUP 9 BSPHA C1 B. Answer the crossword puzzle 2. Is a nitrofurazone derivative that inhibits the parasite-unique enzyme trypanothione reductase GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O F M U O R M T Y I C M I O N X GROUP 9 BSPHA C1 B. Answer the crossword puzzle 3. Is an orally active halogenated hydroxyquinoline luminal amebecide. GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M U O R M T Y I C M I O N GROUP 9 BSPHA C1 X B. Answer the crossword puzzle 4. Is used in combination with sulfamethoxazole as the first choice in prophylaxis and treatment of pneumocystis pneumonia GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M T U O R R M I T Y M I C E M I T O N H X GROUP 9 BSPHA C1 O P R I M B. Answer the crossword puzzle 5. Undergoes a reductive bioactivation of its nitro group by ferredoxin to form reactive cytotoxic products. GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M T M U O R E R M I T T Y M R I C E O M I T N O N H I X GROUP 9 BSPHA C1 O D P A R Z I O M L E B. Answer the crossword puzzle 6. Selective inhibitor of protozoan dihydrofolate reductase GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M T M P U O R E Y R M I T R T Y M R I I C E O M M I T N E O N H I T X GROUP 9 BSPHA C1 O D H P A A R Z M I O I M L N E E B. Answer the crossword puzzle 7. An antimalarial drug that causes Cinchonism GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M T M P Q U I N I N E O R E Y R M I T R T Y M R I I C E O M M I T N E O N H I T X GROUP 9 BSPHA C1 O D H P A A R Z M I O I M L N E E B. Answer the crossword puzzle 8. This tetracycline is a chemoprophylactic for travelers to geographical areas with multidrug resistant P. falciparum. GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N O L F M T M P Q U I N I N E O R D E Y R M I O T R T Y M X R I I C E Y O M M I T C N E O N H Y I T X GROUP 9 BSPHA C1 O C D H P L A A R I Z M I N O I M E L N E E B. Answer the crossword puzzle 9. Primary drug in all forms of leishmaniasis GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N OL F M T M P QU I N I N E O R D E Y R M I O T R T Y M X R I I C E Y O M M S O D I U M S T I B O G L U C ON A T E O N H Y I T X O GROUP 9 BSPHA C1 C D H P L A A R I Z M I N O I M E L N E E B. Answer the crossword puzzle 10. Is an organic arsenical; drug of choice in African sleeping sickness. GROUP 9 BSPHA C1 B. Answer the crossword puzzle P A N R I O D O Q U I N OL F M T M P QU I N I N E O R D E Y R M I O T R T Y M X R I I C E Y O M M S O D I U M S T I B O G L U C ON A T E O N H Y I T X O GROUP 9 BSPHA C1 C D H P L A A M E L A R S O P R O L I Z M I N O I M E L N E E C. Learning Evaluation questions 1. Plasmodial resistance to chloroquine is due to A. Change in receptor structure B. Decreased accumulation of the drug in the food vacuole C. Increased activity of DNA repair mechanisms GROUP 9 BSPHA C1 D. Increased synthesis of dihydrofolate reductase E. Induction of drug-inactivating enzymes C. Learning Evaluation questions 1. Plasmodial resistance to chloroquine is due to A. Change in receptor structure B. Decreased accumulation of the drug in the food vacuole C. Increased activity of DNA repair mechanisms GROUP 9 BSPHA C1 D. Increased synthesis of dihydrofolate reductase E. Induction of drug-inactivating enzymes C. Learning Evaluation questions 2. After the acute infection, which of the following medications is given to treat the asymptomaticcolonization state of E. histolytica? A. Chloroquine. B. Iodoquinol. GROUP 9 BSPHA C1 C. Metronidazole. D. Primaquine C. Learning Evaluation questions 2. After the acute infection, which of the following medications is given to treat the asymptomaticcolonization state of E. histolytica? A. Chloroquine. B. Iodoquinol. GROUP 9 BSPHA C1 C. Metronidazole. D. Primaquine C. Learning Evaluation questions 3. A group of college students are traveling to a chloroquine-resistant malaria area for a mission trip. Which of the following medications can be used for both prevention and treatment of malaria in these students? A. Pyrimethamine. GROUP 9 BSPHA C1 B. Artemisinin. C. Atovaquone–proguanil. D. Melarsoprol. C. Learning Evaluation questions 3. A group of college students are traveling to a chloroquine-resistant malaria area for a mission trip. Which of the following medications can be used for both prevention and treatment of malaria in these students? A. Pyrimethamine. GROUP 9 BSPHA C1 B. Artemisinin. C. Atovaquone–proguanil. D. Melarsoprol. C. Learning Evaluation questions 4. An 18-year-old male is diagnosed with (American trypanosomiasis) Chaga’s disease. Which medication would be the best for this patient? A. Nifurtimox. B. Suramin. GROUP 9 BSPHA C1 C. Sodium stibogluconate. D. Metronidazole C. Learning Evaluation questions 4. An 18-year-old male is diagnosed with (American trypanosomiasis) Chaga’s disease. Which medication would be the best for this patient? A. Nifurtimox. B. Suramin. GROUP 9 BSPHA C1 C. Sodium stibogluconate. D. Metronidazole C. Learning Evaluation questions 5. Which statement about antiprotozoal drugs is accurate? A. Chloroquine is an inhibitor of plasmodial dihydrofolate reductase B. Mefloquine destroys secondary exoerythrocytic schizonts C. Primaquine is a blood schizonticide and does not affect secondary tissue schizonts D. Proguanil complexes with double-stranded DNA-blocking GROUP 9 BSPHA C1 replication E. Trimethoprim-sulfamethoxazole is the drug of choice for Pneumocystis jiroveci pneumonia C. Learning Evaluation questions 5. Which statement about antiprotozoal drugs is accurate? A. Chloroquine is an inhibitor of plasmodial dihydrofolate reductase B. Mefloquine destroys secondary exoerythrocytic schizonts C. Primaquine is a blood schizonticide and does not affect secondary tissue schizonts D. Proguanil complexes with double-stranded DNA-blocking GROUP 9 BSPHA C1 replication E. Trimethoprim-sulfamethoxazole is the drug of choice for Pneumocystis jiroveci pneumonia Questions or comments? SWU

Use Quizgecko on...
Browser
Browser