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Lecture 03.2014

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Antivirals, antihelminths, antifungals

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Lecture 03.2014

  1. 1. MBSM 713: BIOCHEMISTRY OF ANTI MICROBIAL AGENTS Lecture Three: 1.1.AntiviralsAntivirals 2.2.AntifungalsAntifungals 3.3.Antihelmitic drugsAntihelmitic drugs Dr. G. Kattam Maiyoh 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 1
  2. 2. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 2
  3. 3. Understanding VirusesUnderstanding Viruses They are different from other MicrobesThey are different from other Microbes Viral replicationViral replication • A virus cannot replicate on its own • It must attach to and enter a host cell • It then uses the host cell’s energy to synthesize DNA, RNA and protein. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 3
  4. 4. Understanding VirusesUnderstanding Viruses Viruses are difficult to kill because they live inside the cells • Any drug that kills a virus MAY also kill cells 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 4
  5. 5. Anti-viral drugsAnti-viral drugs • Certain viruses multiply in the cytoplasm but others do in the nucleus • Most multiplication take place before diagnosis is made 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 6
  6. 6. Anti-Viral drugs • Many antiviral drugs are Purine or Pyrimidine analogs. • Many antiviral drugs are Prodrugs. They must be phosphorylated by viral or cellular enzymes in order to become active. • Most anti-viral agents inhibits active replication so the viral growth resumes after drug removal. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 7
  7. 7. Antivirals how they act Key characteristics of antiviral drugs Able to enter the cells infected with virus Interfere with viral nucleic acid synthesis and/or regulation Some drugs interfere with ability of virus to bind to cells Some drugs stimulate the body’s immune system Best responses to antiviral drugs are in patients with competent immune systems A healthy immune system works synergistically with the drug to eliminate or suppress viral activity 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 8
  8. 8. Antiviral Medications Antiviral drugs  Used to treat infections caused by viruses other than HIV Antiretroviral drugs  Used to treat infections caused by HIV, the virus that causes AIDS 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 9
  9. 9. Antiviral Drugs: Nonretroviral Mechanism of action  Inhibit viral replication (Does not necessarily mean viral DNA replication.) Used to treat non-HIV viral infections  Influenza viruses  HSV (herpes simplex virus), VZV (vericella zoster virus)  CMV (cytomegalovirus)  Hepatitis A, B, C (HAV, HBV, NCV) Adverse Effects  Vary with each drug  Healthy cells are often killed also, resulting in serious toxicities 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 10
  10. 10. Anti-viral drugs • Current anti-viral agents do not eliminate non- replicating or latent virus • Effective host immune response remains essential for the recovery from the viral infection • Clinical efficacy depends on achieving inhibitory conc. at the site of infection within the infected cells 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 11
  11. 11. Anti-viral drugsAnti-viral drugs Stages of viral replication • Cell entry – attachment - penetration • Uncoating • Transcription of viral genome • Translation • Assembly of virion components • Release 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 12
  12. 12. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 13
  13. 13. Anti-viral drugs Anti-herpes virus agents • Acyclovir / Valacyclovir • Famciclovir / Penciclovir • Ganciclovir / Cidofovir • Foscarnet • Trifluridine / Idoxuridine / Vidarabine 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 14
  14. 14. • Valacyclovir is a prodrug of Acyclovir with better bioavailability. • Famciclovir is hydrolyzed to Penciclovir and has greatest bioavailability. • Penciclovir is used only topically whereas Famciclovir can be administered orally. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 15 Features
  15. 15. PHARMACOLOGY OF ACYCLOVIR AND CONGENERS • Acyclovir, Valacyclovir, Ganciclovir, Famciclovir, Penciclovir • All are guanine nucleoside analogs. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 16
  16. 16. Mechanism of action of Acyclovir and congeners : • All drugs are phosphorylated by a viral thymidine-kinase, then metabolized by host cell kinases to nucleotide analogs. • The analog inhibits viral DNA- polymerase • Only actively replicating viruses are inhibited 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 17
  17. 17. • Acyclovir is thus selectively activated in cells infected with herpes virus. • Uninfected cells do not phosphorylate acyclovir. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 18
  18. 18. Mechanism of Action of Acyclovir 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 19
  19. 19. Antiviral spectrum : • Acyclovir: HSV-1, HSV-2, VZV, Shingles. • Ganciclovir / Cidofovir : CMV • Famciclovir : Herpes genitalis and shingles • Foscarnet : HSV, VZV, CMV, HIV • Penciclovir : Herpes labialis 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 20
  20. 20. Pharmacokinetics of Acyclovir : –Oral bioavailability ~ 20-30% –Distribution in all body tissues including CNS –Renal excretion: > 80% –Half lives: 2-5 hours –Administration: Topical, Oral , IV 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 21
  21. 21. Adverse effects of Acyclovir / Ganciclovir • Nausea, vomiting and diarrhea • Nephrotoxicity - crystalluria, haematuria, renal insufficiency • Myelosuppression – Neutropenia and thrombocytopenia – Ganciclovir 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 22
  22. 22. Therapeutic uses : Acyclovir is the drug of choice for: • HSV Genital infections • HSV encephalitis • HSV infections in immunocompromised patient Ganciclovir is the drug of choice for: • CMV retinitis in immunocompromised patient • Prevention of CMV disease in transplant patients CMV = Cytomegalovirus is a serious eye infection of the retina 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 23
  23. 23. Cidofovir : • It is approved for the treatment of CMV retinitis in immunocompromised patients • It is a nucleotide analog of cytosine – no phosphorylation required. • It inhibits viral DNA synthesis • Available for IV, Intravitreal inj, topical • Nephrotoxicity is a major disadvantage. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 24
  24. 24. PHARMACOLOGY OF FOSCARNET • Foscarnet is an inorganic pyrophosphate analog   • It directly inhibits viral DNA and RNA -polymerase and viral reverse transcriptase (it does not require phosphorylation for antiviral activity) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 28
  25. 25. Foscarnet • HSV-1, HSV-2, VZV, CMV and HIV. • Oral bioavailability ~ 10-20% • Distribution to all tissues including CNS • Administration: IV 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 29
  26. 26. Adverse effects of Foscarnet • Hypocalcemia and hypomagnesemia (due to chelation of the drug with divalent cations) are common. • Neurotoxicity (headache, hallucinations, seizures) • Nephrotoxicity (acute tubular nephrosis, interstitial nephritis) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 30
  27. 27. Therapeutic uses of Foscarnet • It is an alternative drug for • HSV infections (acyclovir resistant / immunocompromised patient ) • CMV retinitis (ganciclovir resistant / immunocompromised patient ) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 31
  28. 28. Respiratory viral infections Influenza – • Amantadine / Rimantadine • Oseltamivir / Zanamavir RSV bronchiolitis – • Ribavirin 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 32
  29. 29. Amantadine and Rimantadine : Influenza • Prevention & Treatment of influenza A • Inhibition of viral uncoating by inhibiting the viral membrane protein M2 • Amantadine has anti-parkinsonian effects. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 33
  30. 30. Pharmacokinetics of Amantadine • Oral bioavailability ~ 50-90% • Amantadine cross extensively BBB whereas Rimantadine does not cross extensively . • Administration: Oral 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 34
  31. 31. Neuraminidase inhibitors : Influenza Oseltamivir / Zanamavir • Influenza contains an enzyme neuraminidase which is essential for the replication of the virus. • Neuraminidase inhibitors prevent the release of new virions and their spread from cell to cell. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 35
  32. 32. Neuraminidase inhibitors : Influenza Oseltamivir / Zanamavir • These are effective against both types of influenza A and B. • Do not interfere with immune response to influenza A vaccine. • Can be used for both prophylaxis and acute treatment. Administration • Oseltamivir is orally administered. • Zanamavir is given intranasal. 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 36
  33. 33. Viru s       Diseases Drug(s) of choice Alternative drugs FLU A   Influenza Amantadine Rimantadine RSV Pneumonia, bronchiolitis Ribavirin (aerosol)   HSV   Genital herpes Acyclovir Foscarnet     Keratitis Conjunctivitis Trifluridine Idoxuridine Vidarabine   Encephalitis Acyclovir     Neonatal HSV infection Acyclovir Vidarabine   Herpes infections in immuno- compromised host Acyclovir Foscarnet 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 48
  34. 34. VZV     In normal host No therapy   In immunocompro- mised host, or during pregnancy Acyclovir Foscarnet CMV Retinitis Ganciclovir Foscarnet HIV AIDS HIV antibody positive with CD4 count < 500/mm3 Zidovudine ± protease inhibitors Didanosine, Stavudine HBV HCV Hepatitis B, C Interferons   01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 49
  35. 35. Antiretroviral Drugs HAART - Highly active antiretroviral therapy • Includes at least three medications –“cocktails” • These medications work in different ways to reduce the viral load 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 50
  36. 36. Antiretroviral Drugs • Reverse transcriptase inhibitors (RTIs) – Block activity of the enzyme reverse transcriptase, preventing production of new viral DNA • Include: – Nucleoside RTIs (NRTIs) – Nonnucleoside RTIs (NNRTIs) – Nucleotide RTIs (NTRTIs) • Examples abacavir (Ziagen) delavirdine (Rescriptor) didanosine (Videx) lamivudine (Epivir) stavudine (Zerit) tenofovir (Viread) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 51
  37. 37. Antiretroviral Drugs • Protease inhibitors (PIs) – Inhibit the protease a retroviral enzyme, preventing viral replication – Examples: amprenavir (Agenerase) indinavir (Crixivan) nelfinavir (Viracept) ritonavir (Norvir) saquinavir (Invirase) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 52
  38. 38. Antiretroviral DrugsAntiretroviral Drugs • Fusion inhibitors – Inhibit viral fusion, preventing viral replication – Newest class of antiretroviral drugs – Example: enfuvirtide (Fuzeon) 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 53
  39. 39. Antiretroviral Drugs • Combinations of multiple antiretroviral medications are common • Adverse effects vary with each drug and may be severe−monitor for dose- limiting toxicities • Monitor for signs of opportunistic diseases 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 54
  40. 40. Antiretroviral Drugs:Antiretroviral Drugs: Adverse EffectsAdverse Effects  Numerous and varyNumerous and vary with each drugwith each drug Drug therapy may need to be modified because of adverse effects Goal is to find the regimen that will best control the infection with a tolerable adverse effect profile  Medication regimens change during the course of the illnessduring the course of the illness 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 55 Antiviral DrugsAntiviral Drugs
  41. 41. ANTIFUNGAL DRUGS Systemic & Topical Some are fungistatic, while others are fungicidal 01/23/15 56 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  42. 42. Fungal Infection in Humans = Mycosis Fungal Infection in Humans = Mycosis • Major Types of Mycoses – superficial – cutaneous – subcutaneous – systemic – opportunistic • Symptoms vary from cosmetic to life threatening 01/23/15 57 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  43. 43. Antifungal Agents • Polyene antibiotic • The polyene antibiotics bind with sterols in the fungal cell membrane, principally ergosterol. This causes the cell's contents to leak out and the cell dies. Animal cells contain cholesterol instead of ergosterol and so they are much less susceptible. – Nystatin – Amphotericin B (may be administered liposomally) – Natamycin – Rimocidin – Filipin – Pimaricin 01/23/15 58 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  44. 44. Antifungal Agents Imidazole and triazole • The imidazole and triazole groups of antifungal drugs inhibit the enzyme cytochrome P450 14α- demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell membrane synthesis. These drugs also block steroid synthesis in humans. • Imidazoles: • Miconazole Bifonazole • Ketoconazole Butoconazole • Clotrimazole Econazole • Mebendazole Fenticonazole • Isoconazole Oxiconazole • Sertaconazole Sulconazole • Thiabendazole Tiaconazole01/23/15 60 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  45. 45. Antifungal Agents • The triazoles are newer, and are less toxic and more effective: • Fluconazole • Itraconazole • Ravuconazole • Posaconazole • Voriconazole 01/23/15 61 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  46. 46. Antifungal Agents Allylamines • Allylamines inhibit the enzyme squalene epoxidase, another enzyme required for ergosterol synthesis: – Terbinafine - marketed as Lamisil – Amorolfine – Naftifine – Butenafine 01/23/15 62 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  47. 47. Antifungal Agents Echinocandin • Echinocandins inhibit the synthesis of glucan in the cell wall, probably via the enzyme 1,3-β glucan synthase: – Anidulafungin – Caspofungin – Micafungin 01/23/15 63 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  48. 48. Antifungal Agents • Others: –Flucytosine is an antimetabolite. –Griseofulvin binds to polymerized microtubules and inhibits fungal mitosis; It is derived from the mold Penicillium griseofulvum. –Fluocinonide –Salicylic Acid (topical) –Tinactin or Tolnaftate –Potassium Iodide 01/23/15 64 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03
  49. 49. ANTHELMINTIC DRUGS 01/23/15 GKM/KISIIU/MBSM713 /BIOC.AMIC.AGENS.LEC03 65
  50. 50. Helminth Infections 1-Tapeworms ( cestodes) Beef tapeworm / fish tapeworm 2- Intestinal round worms ( nematodes) Ascaris, pinworm ,whipworm, strongyloides, ancylostoma ( hookworm ). A skin infection is termed cutaneous larva migrans
  51. 51. Mechanism of action • May act by causing : • 1- paralysis of the worm. • 2- damaging the worm leading to partial digestion or rejection by immune mechanisms. • 3- interfere with the metabolism of the worm. *Worms or larvae live in tissues of host body like muscles , viscera , menninges , subcutaneous tissues.
  52. 52. • Adult filariae live in the lymphatics, connective tissue or mesentery of host and produce live embryos or microfilariae, which goes to blood stream. • They are ingested by mosquitoes or similar insects, they develop to larvae this secondary host and pass to mouth parts of insect and re-injected to humans
  53. 53. Ascaris lumbricoids ( common round worm)
  54. 54. ANTHELMINTIC DRUGS ALBENDAZOLE • Broad spectrum oral anthelmintic • Drug of choice for treatment of hydatid disease (tapeworm) and cysticercosis (pork tapeworm) • It is also used for the treatment of ascariasis ,tricurasis and strongyloidiasis, pinworm, hookworm
  55. 55. Mechanism Of Action 1. Inhibits microtubule synthesis by binding to β – tubulin. 2. Inhibits mitochondrial reductase causing reduced glucose transport. Intestinal parasites are immobilized and die slowly. • Larvicidal in hydatid ,cysticercosis , ascariasis and hook worm infections. • Ovicidal in ascariasis, hookworm ,trichuriasis
  56. 56. Pharmacokinetics • Formulated as Benzimidazole carbamate • Administered orally , absorption increased with a fatty meal • Metabolized in the liver to the active metabolite called albendazole sulfoxide
  57. 57. Pharmacokinetics • Plasma half life is 8-12 hours • sulfoxide is mostly protein bound distributes well to tissues and enters bile,CSF & hydatid cysts. • Metabolites are excreted in urine
  58. 58. Clinical uses • Used on empty stomach when used against intraluminal parasites but with a fatty meal when used against tissue parasites. 1. In ascariasis ,trichuriasis ,hookworm, pin worm infections : 2. Hydatid diseases
  59. 59. Albendazole (con’) 3. Neurocysticercosis: Used with corticosteroid to decrease the inflammation caused by dying organism and it also reduces the duration of course for 21 days 4. Other infections: Drug of choice in cutaneous and visceral larva migrans , intestinal capillariasis, giardiasis & taeniasis.
  60. 60. Adverse Effects • In short term(1-3 days): Mild epigastric pain,diarrhea, nausea, headache & insomnia. • In long term use : for hydatid cyst and cysticercosis : abdominal pain, headache ,fever ,fatigue, alopecia , increased liver enzymes , pancytopenia. Blood counts and liver enzymes should be followed. • Not given during pregnancy, hypersensitive people to benzimidazole drugs & children under 2 years .
  61. 61. PYRANTEL PAMOATE • Broad spectrum • Pharmacokinetics: – Poorly absorbed from GIT – Half of the drug is excreted unchanged in the feces. • Mechanism of action: – result in paralysis of worms. It is a neuromuscular blocking agent Efficacy – Very effective against luminal organisms( mature or immature forms). – Not effective against migratory stages in the tissues or against ova
  62. 62. Clinical uses • Pin worm given orally with or without food. • Ascariasis • Hookworm Pinworm male ,female
  63. 63. Adverse Effects Infrequent mild transient GI disturbance – Drowsiness , headache ,insomnia. – Rash ,fever Contraindications & Cautions – Should be used with caution in liver dysfunction. – Pregnancy – Children under 2 years of age
  64. 64. PIPERAZINE • Only recommended for the treatment of ascariasis • Cure rate 90% for 2 days treatment. • Readily absorbed orally and excreted mostly unchanged in urine • Mechanism of action: Causes paralysis of ascaris by blocking acetylcholine at myoneural junction , the live worms expelled by normal peristalsis. • Treatment • Treatment is continued for 3-4 days or repeated after one week in case of heavy infections.
  65. 65. Adverse Effects • GI disturbance • Neurotoxicity ,allergic reactions . • Contraindications • Epilepsy or a history of epilepsy • Impaired liver or kidney functions • pregnancy • Chronic neurologic disease
  66. 66. NICLOSAMIDE • Second-line drug for treatment of most tapeworm infections. • Mechanism of action: • Adult worm( not ova) is rapidly killed by inhibition of oxidative phosphorylation . • Pharmacokinetics: • Poorly absorbed from gut & excreted in urine.
  67. 67. Clinical Uses • Treatment of most forms of tapeworms. • Not effective against cysticercosis or hydatic disease. • Given in the morning on empty stomach. • Purgative is necessary to purge all dead segments& prevent liberation of ova.
  68. 68. Adverse effects & Contraindications • Mild ,infrequent and transitory GI disturbance • Alcohol consumption should be avoided • Not indicated in children under 2 years of age or in pregnancy.
  69. 69. DIETHYL CARBAMAZINE • Drug of choice for the treatment of filariasis and tropical eosinophilia. • Pharmacokinetics: • Rapidly absorbed from gut • Half- life is 2-3 hours • The drug should be given after meals • It is excreted in urine as unchanged or metabolite. • Dosage is reduced in urinary alkalosis and renal impairment.
  70. 70. Mechanism Of Action • Immobilizes microfilariae and alters their surface structure ,displacing them from tissues & making them susceptible to destruction by host defense mechanism • It has immunosuppressive effects
  71. 71. Adverse Effects • Fever , malaise, papular rash, headache, GI disturbance,cough. Chest,muscle,joint pain • Leucocytosis • Retinal hemorrhage • Encephalopathy • lymphangitis and lymphadenopathy. • *It is not teratogenic
  72. 72. Contraindications & Cautions • * Hypertension • * Renal disease * Patient with lymphangitis
  73. 73. IVERMECTIN • Drug of choice for treatment of strongyloidiasis • Macrocyclic lactone ring • Given only orally • Rapidly absorbed • Does not cross BBB. • Half- life is 16 hrs • Excretion is mainly in feces.
  74. 74. Mechanism Of Action • Acts on the parasitte, s glutamate-gated Cl- channel receptors . Chloride influx increased , hyperpolarization occurs , resulting in paralysis of the worm. Or • Paralyze nematodes by intensifying GABA- mediated transmission of signals in peripheral nerves.
  75. 75. Clinical uses • Drug of choice for cutaneous larva migrans & strongyloidiasis. • Onchocerciasis • It is also used for scabies , lice . • Filariasis.
  76. 76. Adverse Effects • Fatigue ,dizziness, GI disturbance • Killing of microfilaria result in a Mazotti reaction ( fever, headache, dizziness, somnolence, hypotension , tachycardia, peripheral edema……). • Corneal opacities & other eye lesions.
  77. 77. Contraindications & Cautions • Concomitant use with other drugs that enhance GABA e.g Barbiturates, bnzodiazepines, valproic acid. • pregnancy • Meningitis • Children under 5 years of age.
  78. 78. BITHIONOL • Drug of choice for the treatment of fascioliasis ( sheep liver fluke) • Pharmacokinetics: • It is orally administered and excreted in urine.
  79. 79. Adverse Effects • GI disturbance ( N., V., D., A.) Dizziness, headache Skin rashes , urticaria, Leucopenia • Contraindications and precautions: Hepatitis , leucopenia Used with caution in children under 8 years of age.

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