ANTIFUNGALS

1. ANTIFUNGALS Fungus-------single cell organism with cell wall has chitin, no chlorophyhll. reproduction by spores. study is mycology most are resistant to antibacterial drugs. Infection occurs when immune system is compromised. microorganisms such as yeasts and molds, mushrooms MOA: Antifungals work by exploiting differences between mammalian and fungal cells to kill the fungal organism with fewer adverse effects to the host. Unlike bacteria, both fungi and humans are eukaryotes. Thus, fungal and human cells are similar at the biological level. This makes it more difficult to discover drugs that target fungi without affecting human cells. As a consequence, many antifungal drugs cause side effects. Some of these side effects can be life-threatening if the drugs are not used properly.

2. ANTIFUNGALS-polyeneantimycotic • attack cell membrane, similar structure Amphotericin B, nystatin, and natamycin nystatin used mostly topical. amphotericin used intravenous unless fungus inside GI. reactions---fever, chills, rigor, nausea,vomiting, myalgias, arthralgias, and headache during intravenous infusions. renal damage

3. ANTIFUNGALS=azoles • interferes with enzyme for ergosterol formation yields death. • used for ringworm, candidiasis • clotrimazole, miconazole, ketoconazole,fluconazole • side effects--naseau, diarrhea, rashes, liver issues

4. ANTIFUNGALS--griseofulvin • from Penicillium griseofulvum • attacks dermatophytes by disrupting mitotic spindle formation-a critical step in cellular division. • for severe skin,hair, nails condition. • not topical use • oral use 2 to 4 weeks for skin infections, 4 to 6 weeks for hair and scalp infections, 4 to 8 weeks for foot infections, 3 to 4 months for fingernail infections, and at least 6 months for toenail infections.

5. ANTIVIRALS • Viruses have no cell wall and made up of nucleic acid components • Viruses are obligate intracellular parasite • They do not have a metabolic machinery of their own – uses host enzymes • virus can be attacked somewhere along its reproduction pathway.

6. ANTIVIRALS • most replication when symptoms appear or before • viral replication • 1--penetrates cell • 2--synthesis of early protein • 3--synthesis of RNA or DNA • 4--synthesis of late protein • 5--particle assembly and release=cell death

7. ANTIVIRALS • gamma globulin injection--blood protein with antibodies hopefully act against virus antigen to not allow entry into cell. • to reduce infection of measles, rabies, others • amantadine--(CDC sometimes disapproves) prevents uncoating of virus • for influenza A, rubella. • maybe useful for chronic fatigue • side effects---slurred speech, dizziness

8. ANTIVIRALS • stopping intracelluar synthesis • ribavarin---inhibits replication of DNA and RNA virus • for hepatitus C, respiratory infections, hemmoraghic fever • acyclovir--metabolized into a form that replaces a nucleotide=no more dna (AGTC) • for herpes simplex and zoster

9. ANTIVIRALS • interferon--protein that dying cell releases so other cells can produce enzyme that reduces RNA. • for hepatitus B and C, and cancers

10. ANTIVIRALS • florophenylalanine---inhibit late protein synthesis • inhibit protein coat for virus • also destroys cell protein so too toxic.

11. ANTIVIRALS • inhibit final assembly • use puromycin antibiotic that causes defective protein=no protein virus coat