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Educational Objective:
Educational Objective:
Cerebral toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year.  Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor.
Cerebral toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year.  Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor.
|AnswerA=Inhibition of heme polymerase activity
|AnswerA=Inhibition of heme polymerase activity
|AnswerAExp=Chloroquine, an antimalarial drug, is a plasmodium heme polymerase inhibitor.
|AnswerAExp=Chloroquine, an antimalarial drug, is a plasmodium heme polymerase inhibitor.
|AnswerB=Inhibition of dihydrofolate reductase activity
|AnswerB=Inhibition of dihydrofolate reductase activity
|AnswerBExp=Pyrimethamine, a drug used to treat toxoplasmosis, is a dihydrofolate reductase inhibitor.
|AnswerBExp=Pyrimethamine, a drug used to treat toxoplasmosis, is a dihydrofolate reductase inhibitor.
|AnswerC=Free radical toxicity of organism’s DNA  
|AnswerC=Free radical toxicity of organism’s DNA
|AnswerCExp=Metronidazole, an antibiotic and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA
|AnswerCExp=Metronidazole, an antibiotic and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA
|AnswerD=Blockade of peptide bond formation at 50S ribosomal subunit  
|AnswerD=Blockade of peptide bond formation at 50S ribosomal subunit
|AnswerDExp=Several antibiotics, including chloramphenicol, macrolides, clindamycin, streptogramins, and linezolid, block peptide bond formation at 50S ribosomal subunit.
|AnswerDExp=Several antibiotics, including chloramphenicol, macrolides, clindamycin, streptogramins, and linezolid, block peptide bond formation at 50S ribosomal subunit.
|AnswerE=Inhibition of DNA polymerase activity
|AnswerE=Inhibition of DNA polymerase activity
|AnswerEExp=Antiviral medications, such as acyclovir, ganciclovir, foscarnet, and cidofovir are DNA polymerase inhibitors.  
|AnswerEExp=Antiviral medications, such as acyclovir, ganciclovir, foscarnet, and cidofovir are DNA polymerase inhibitors.
|RightAnswer=B
|RightAnswer=B
|WBRKeyword=Toxoplasma, gondii, toxomplasmosis, HIV, seizure, ring, enhancing, lesion, pyrimethamine, dihydrofolate, reductase, inhibitor
|WBRKeyword=Toxoplasma gondii, toxomplasmosis, HIV, seizure, ring enhancing lesion, pyrimethamine, dihydrofolate reductase inhibitor
|Approved=No
|Approved=No
}}
}}

Revision as of 12:06, 16 September 2013

 
Author [[PageAuthor::Rim Halaby, M.D. [1]]]
Exam Type ExamType::USMLE Step 1
Main Category MainCategory::Microbiology
Sub Category SubCategory::Neurology
Prompt [[Prompt::A 28 year old HIV-positive female patient presents to the emergency department with high grade fever, headache, and new onset tonic-clonic seizures. The patient also explains she has been anorexic and very weak recently. Laboratory work-up reveals CD4 count = 80 cells/µL per year. Head computer tomography (CT) scan shows multiple ring enhancing lesions in the frontal lobes. The patient requires treatment with a medication that has which of the following mechanisms of action?]]
Answer A AnswerA::Inhibition of heme polymerase activity
Answer A Explanation AnswerAExp::Chloroquine, an antimalarial drug, is a plasmodium heme polymerase inhibitor.
Answer B AnswerB::Inhibition of dihydrofolate reductase activity
Answer B Explanation AnswerBExp::Pyrimethamine, a drug used to treat toxoplasmosis, is a dihydrofolate reductase inhibitor.
Answer C AnswerC::Free radical toxicity of organism’s DNA
Answer C Explanation AnswerCExp::Metronidazole, an antibiotic and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA
Answer D AnswerD::Blockade of peptide bond formation at 50S ribosomal subunit
Answer D Explanation AnswerDExp::Several antibiotics, including chloramphenicol, macrolides, clindamycin, streptogramins, and linezolid, block peptide bond formation at 50S ribosomal subunit.
Answer E AnswerE::Inhibition of DNA polymerase activity
Answer E Explanation AnswerEExp::Antiviral medications, such as acyclovir, ganciclovir, foscarnet, and cidofovir are DNA polymerase inhibitors.
Right Answer RightAnswer::B
Explanation [[Explanation::Cerebral toxoplasmosis is caused by Toxoplasma gondii, an opportunistic parasitic infection that often infects HIV-positive patients with CD4 counts < 100 cells/µL per year. Toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient. Multiple ring-enhancing lesions on head CT scan are characteristic. Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor.

Educational Objective: Cerebral toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year. Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor.
Educational Objective:
References: ]]

Approved Approved::No
Keyword WBRKeyword::Toxoplasma gondii, WBRKeyword::toxomplasmosis, WBRKeyword::HIV, WBRKeyword::seizure, WBRKeyword::ring enhancing lesion, WBRKeyword::pyrimethamine, WBRKeyword::dihydrofolate reductase inhibitor
Linked Question Linked::
Order in Linked Questions LinkedOrder::