Anti-Infectives PDF

ANTI INFECTIVES IMMUNE SYSTEM AND INFECTION Physical Barriers □Skin: The first line of defense, acting as a physical and mechanical barrier to block pathogen entry. □Mucous Membranes: Found in the respiratory, gastrointestinal, and urogenital tracts, they trap pathogens in mucus and expel them...

ANTI INFECTIVES IMMUNE SYSTEM AND INFECTION Physical Barriers □Skin: The first line of defense, acting as a physical and mechanical barrier to block pathogen entry. □Mucous Membranes: Found in the respiratory, gastrointestinal, and urogenital tracts, they trap pathogens in mucus and expel them via sneezing, coughing, or cilia action. □Stomach Acid: The acidic pH of the stomach neutralizes ingested microorganisms, providing a chemical barrier. IMMUNE SYSTEM AND INFECTION Innate Immunity □ Non-Specific Defense: The innate immune system responds quickly and indiscriminately to invading pathogens. Key Components: ✔ Macrophages and Neutrophils: Phagocytic cells that engulf and digest pathogens. ✔ Natural Killer (NK) Cells: Destroy virus-infected cells and tumor cells. ✔ Complement System: A cascade of proteins that tag pathogens for destruction, directly kill them, or enhance inflammation. IMMUNE SYSTEM AND INFECTION Adaptive Immunity □ Specific Defense: Targets specific antigens and provides long- term immunity. Key Components a. T-Cells: ✔ Helper T-cells activate other immune cells. ✔ Cytotoxic T-cells destroy infected cells. b. B-Cells: Produce antibodies that neutralize pathogens or mark them for destruction by other immune cells. c. Memory Cells: Ensure a faster and stronger response upon re- exposure to the same pathogen.  PATHOPHYSIOLOGY The inflammatory process is a vital response of the immune system to injury or infection, aiming to eliminate the cause of harm, clear damaged cells, and initiate tissue repair. The classic signs of inflammation, often referred to as the cardinal signs, are Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), and sometimes Functio Laesa (loss of function). Sequence of Events in Inflammation 1. Injury or Infection: Triggers the release of inflammatory mediators from cells like mast cells, macrophages, and damaged tissues. 2. Vasodilation: Blood vessels widen, leading to redness (rubor) and heat (calor). 3. Increased Vascular Permeability: Plasma and immune cells move into tissues, causing swelling (tumor). 4. Recruitment of Immune Cells: Neutrophils and macrophages migrate to the site via chemotaxis. 5. Pain Mediators: Chemical signals like bradykinin and prostaglandins stimulate pain (dolor). 6. Tissue Repair: Immune cells clear debris and pathogens, and the tissue begins to heal. PATHOPHYSIOLOGY Bacterial Infections ✔ Mechanism: Pathogenic bacteria invade host tissues and replicate. ✔ Toxins: ✔ Exotoxins: Proteins secreted by bacteria that damage host cells (e.g., diphtheria toxin). ✔ Endotoxins: Components of the bacterial cell wall (e.g., lipopolysaccharides) that trigger strong immune responses. ✔ Effects: Tissue damage, inflammation, and sepsis in severe cases. Viral Infections ✔ Mechanism: Viruses enter host cells, hijack cellular machinery to replicate, and often destroy the host cells in the process. ✔ Immune Response: ✔ Cytotoxic T-cells target infected cells. ✔ Interferons inhibit viral replication. ✔ Effects: Range from mild symptoms (e.g., colds) to life-threatening conditions (e.g., COVID-19). PATHOPHYSIOLOGY Fungal Infections ✔ Mechanism: Fungi can invade tissues or grow on mucous membranes and skin. ✔ Susceptibility: Immunocompromised individuals (e.g., those with HIV/AIDS or on immunosuppressive therapy) are at higher risk. ✔ Examples: Candidiasis, aspergillosis, and ringworm. Parasitic Infections ✔ Mechanism: Parasites such as protozoa (e.g., Plasmodium causing malaria) or helminths (e.g., tapeworms) invade host tissues or live within the gastrointestinal tract. ✔ Effects: Nutritional deficiencies, immune system exhaustion, and tissue damage. Anti-Infective Agents Anti-infective agents combat infections by targeting specific pathogens. They include: Antibiotics Target bacteria by disrupting cell walls, protein synthesis, DNA replication, or metabolic pathways. Examples: Penicillins, tetracyclines, and fluoroquinolones. Antivirals Inhibit viral replication or entry into host cells. Examples: Acyclovir (for herpesvirus), oseltamivir (for influenza). Antifungals Target fungal cell membranes or inhibit their growth. Examples: Amphotericin B, fluconazole. Antiprotozoals and Anthelmintics Protozoa: Metronidazole targets DNA synthesis in parasites like Giardia and Trichomonas. Helminths: Albendazole disrupts worm metabolism. I. Antibiotics are drugs used to prevent and treat bacterial infections by either killing bacteria (bactericidal) or inhibiting their growth and replication (bacteriostatic). CLASSIFICATION : A. MECHANISM OF ACTION B. CHEMICAL STRUCTURE C. SPECTRUM ACTIVITY D. TARGET PATHOGEN 1. Classification Based on Mechanism of Action A. Inhibition of Cell Wall Synthesis These antibiotics target the bacterial cell wall, which is essential for maintaining structural integrity. Examples: Beta-lactams: Penicillins, cephalosporins, carbapenems, monobactams. Glycopeptides: Vancomycin, teicoplanin. ✔ Inhibit enzymes involved in peptidoglycan synthesis, weakening the cell wall and causing lysis. ✔ Effective against Gram-positive bacteria and some Gram-negative organisms. 1. Classification Based on Mechanism of Action B. Inhibition of Protein Synthesis These antibiotics bind to bacterial ribosomes and interfere with protein synthesis. Examples: Aminoglycosides (e.g., gentamicin, amikacin) – Bind to 30S ribosome. Tetracyclines (e.g., doxycycline, minocycline) – Block tRNA binding to the 30S ribosome. Macrolides (e.g., erythromycin, azithromycin) – Target the 50S ribosome. Chloramphenicol – Inhibits peptidyl transferase in the 50S subunit. Broad-spectrum, often used for atypical bacteria like Mycoplasma and Chlamydia. 1. Classification Based on Mechanism of Action C. Inhibition of Nucleic Acid Synthesis These antibiotics interfere with DNA or RNA synthesis. Examples: Quinolones/Fluoroquinolones (e.g., ciprofloxacin, levofloxacin): Inhibit DNA gyrase and topoisomerase IV. Rifamycins (e.g., rifampin): Inhibit RNA polymerase. Metronidazole: Causes DNA strand breaks in anaerobic bacteria. ✔ Effective against a range of Gram-negative and some Gram-positive bacteria. 1. Classification Based on Mechanism of Action D. Disruption of Cell Membrane Integrity These antibiotics increase membrane permeability leading to cell death. Examples: Polymyxins (e.g., colistin): Target Gram-negative bacteria. Daptomycin: Effective against Gram-positive bacteria. ✔ Often reserved for multidrug-resistant bacteria. 1. Classification Based on Mechanism of Action E. Inhibition of Metabolic Pathways These antibiotics disrupt essential bacterial metabolic processes, such as folate synthesis. Examples: Sulfonamides: Inhibit dihydropteroate synthase. Trimethoprim: Inhibits dihydrofolate reductase. ✔ Used for urinary tract infections (UTIs) and respiratory infections. 2. CLASSIFICATION OF ANTIBIOTICS BASED ON CHEMICAL STRUCTURE 1. Beta-Lactams These antibiotics inhibit bacterial cell wall synthesis. A. Penicillins ✔ Natural Penicillins: Penicillin G, Penicillin V. ✔ Aminopenicillins: Amoxicillin, Ampicillin. ✔ Anti-staphylococcal Penicillins: Nafcillin, Oxacillin, Dicloxacillin. ✔ Extended-Spectrum Penicillins: Piperacillin, Ticarcillin. ✔ Beta-lactamase Inhibitor Combinations: Amoxicillin-clavulanate, Piperacillin- tazobactam. Indications: Severe infections by Streptococcus pyogenes, Streptococcus pneumoniae, Treponema pallidum (syphilis), Clostridium perfringens (gas gangrene). Mild to moderate streptococcal infections (pharyngitis, tonsillitis), dental infections. S/E: Rash, anaphylaxis Nausea, diarrhea. Pain at injection site (Penicillin G). B. Cephalosphorins A. 1st Generation Cephalosporins ✔ Excellent activity against Gram-positive cocci (e.g., Staphylococcus aureus, Streptococcus pyogenes). ✔ Limited activity against Gram-negative bacteria (E. coli, Klebsiella pneumoniae). Examples: Cefazolin (IV/IM) Cephalexin (oral) Cefadroxil (oral) Indications : Surgical prophylaxis (e.g., cefazolin) Skin and soft tissue infections. Urinary tract infections (UTIs). Minimal CNS penetration; not used for meningitis. B. 2nd Generation Cephalosporins ✔ Broader Gram-negative activity compared to the 1st generation. ✔ Effective against H. influenzae, Neisseria spp., and Proteus mirabilis. ✔ Less potent against Gram-positive organisms than 1st generation. Examples: Cefuroxime (IV/IM, oral), Cefaclor (oral), Cefoxitin and Cefotetan (IV/IM; cephamycins with anaerobic activity). Indications : Respiratory tract infections, Sinusitis and otitis media, Mixed anaerobic infections (e.g., peritonitis, pelvic inflammatory disease).Limited CNS penetration. B. CEPHALOSPHORINS C. 3rd Generation Cephalosporins ✔ Enhanced activity against Gram-negative bacteria (Enterobacteriaceae, Neisseria gonorrhoeae, H. influenzae). ✔ Reduced activity against Gram-positive cocci compared to earlier generations (except ceftriaxone). Examples: Ceftriaxone (IV/IM). Cefotaxime (IV/IM) Ceftazidime (IV/IM; active against Pseudomonas aeruginosa) Cefixime (oral). Indications : Serious infections: sepsis, pneumonia, meningitis (good CNS penetration). Gonorrhea (ceftriaxone) Intra-abdominal and urinary tract infections Pseudomonal infections (ceftazidime). Widely used but resistance (e.g., ESBL-producing bacteria) is a concern. B. CEPHALOSPHORINS D. 4th Generation Cephalosporins ✔ Broad spectrum with enhanced Gram-negative coverage, including Pseudomonas aeruginosa. ✔ Retains strong Gram-positive activity (Streptococcus, Staphylococcus). ✔ More resistant to beta-lactamases compared to 3rd generation. Examples: Cefepime (IV/IM). Indications : Nosocomial infections: pneumonia, febrile neutropenia, sepsis. Multidrug-resistant Gram-negative infections. Effective in CNS infections; considered more stable against resistance mechanisms. E. 5th Generation Cephalosporins ✔ Active against multidrug-resistant Gram-positive bacteria, including MRSA (Methicillin- resistant Staphylococcus aureus). ✔ Retains good Gram-negative activity (excluding Pseudomonas). Examples: Ceftaroline (IV). Ceftobiprole (IV; not approved in all countries). Indications : MRSA-related infections. Community-acquired pneumonia (CAP). Skin and soft tissue infections. Often reserved for resistant infections due to its advanced activity. C. Carbapenems Imipenem, Meropenem, Ertapenem, Doripenem. D. Monobactams : Aztreonam. 2. Aminoglycosides These antibiotics inhibit bacterial protein synthesis (30S ribosome) Ex : Gentamicin, Amikacin, Tobramycin, Streptomycin, Neomycin, Kanamycin. 3. Macrolides These antibiotics inhibit bacterial protein synthesis (50S ribosome). Ex : Erythromycin, Azithromycin, Clarithromycin. 4. Tetracyclines These antibiotics inhibit bacterial protein synthesis (30S ribosome). Ex : Tetracycline, Doxycycline, Minocycline, Tigecycline. 5. Fluoroquinolones These antibiotics inhibit DNA gyrase and topoisomerase IV. Ciprofloxacin, Levofloxacin, Moxifloxacin, Ofloxacin, Norfloxacin. 6. Glycopeptides These antibiotics inhibit bacterial cell wall synthesis. Vancomycin, Teicoplanin, Dalbavancin, Oritavancin. 7. Sulfonamide These antibiotics inhibit folic acid synthesis. Sulfamethoxazole (combined with trimethoprim as co-trimoxazole), Sulfadiazine, Sulfisoxazole. 8. Lincosamides These antibiotics inhibit bacterial protein synthesis (50S ribosome). Clindamycin, Lincomycin. 9. Nitroimidazoles These antibiotics disrupt DNA in anaerobic bacteria and protozoa. Metronidazole, Tinidazole. 10. Polymyxins These antibiotics disrupt bacterial cell membranes. Polymyxin B, Polymyxin E (Colistin). 3. Classification Based on Spectrum of Activity A. Narrow-Spectrum Antibiotics Effective against a specific group of bacteria. Examples: Penicillin G (Gram-positive bacteria), isoniazid (Mycobacterium tuberculosis). B. Broad-Spectrum Antibiotics Effective against a wide range of Gram-positive and Gram- negative bacteria. Examples: Tetracyclines, fluoroquinolones, carbapenems. 4. Classification Based on Target Pathogen A. Gram-Positive Bacteria Drugs: Vancomycin, daptomycin, penicillin. B. Gram-Negative Bacteria Drugs: Colistin, aminoglycosides, fluoroquinolones. C. Atypical Bacteria Drugs: Macrolides, tetracyclines. D. Anaerobic Bacteria Drugs: Metronidazole, clindamycin. SPECIAL CONSIDERATUONS A. Antibiotic Resistance ✔ Enzyme production (e.g., beta-lactamase). ✔ Altered target sites. ✔ Efflux pumps. Examples: Methicillin-resistant Staphylococcus aureus (MRSA), multidrug-resistant Pseudomonas aeruginosa. B. Adverse Effects Common side effects include gastrointestinal disturbances, allergic reactions, nephrotoxicity, and ototoxicity. C. Antibiotic Stewardship Ensures appropriate use to reduce resistance. Includes prescribing the right drug, dose, and duration. COMMON S/E : nausea, vomiting, diarrhea, abdominal cramping, and appetite loss. Allergic reactions, including rashes, urticaria (hives), and in severe cases, anaphylaxis, are also frequent, particularly with beta-lactam antibiotics like penicillins and cephalosporins. Overuse or prolonged therapy may lead to superinfections, such as Clostridium difficile-associated diarrhea (CDAD) or fungal infections like oral thrush and vaginal candidiasis. Hematologic side effects, including anemia, leukopenia, or thrombocytopenia, DRUG TO DRUG INTERACTIONS Anticoagulants (e.g., Warfarin): Increased risk of bleeding due to prolonged INR with macrolides, fluoroquinolones, or sulfamethoxazole/trimethoprim. Oral Contraceptives: Reduced efficacy when gut flora is disrupted, necessitating backup contraception. CNS Drugs: Risk of toxicity with certain antibiotics (e.g., increased digoxin levels with macrolides). Theophylline and Other Narrow-Therapeutic-Index Drugs: Elevated levels due to impaired metabolism (e.g., fluoroquinolones inhibiting theophylline clearance). Electrolyte-Altering Drugs: Additive risks with aminoglycosides (nephrotoxicity, ototoxicity) and diuretics. ANTI VIRALS Antiviral medications are a class of drugs specifically designed to treat viral infections by inhibiting the replication and activity of viruses. ✔ Unlike antibiotics, which target bacteria, antivirals selectively act on viruses without significantly harming host cells. ✔ Their development is challenging due to the unique nature of viruses, which rely on host cellular machinery for replication. Mechanism of Action Antivirals target various stages of the viral life cycle: 1. Attachment and Entry Inhibitors: Prevent the virus from binding and entering host cells. Examples: Maraviroc: Blocks the CCR5 receptor for HIV entry. Enfuvirtide: Prevents fusion of the HIV envelope with the host cell membrane. 2. Uncoating Inhibitors: Inhibit the release of viral genetic material into the host cell. Example: Amantadine and Rimantadine: Target influenza A by inhibiting the M2 protein. 3. Nucleic Acid Synthesis Inhibitors: Prevent replication of viral genetic material. Examples: Acyclovir: A guanine analog effective against herpesviruses (e.g., HSV and VZV). Sofosbuvir: Inhibits RNA polymerase in hepatitis C virus (HCV). Remdesivir: Targets the RNA-dependent RNA polymerase of SARS- CoV-2. 4. Integration Inhibitors: Block the integration of viral DNA into the host genome. Example: Raltegravir: Used for HIV treatment. 5. Protein Synthesis and Processing Inhibitors: Target viral enzymes responsible for processing viral proteins. Examples: Ritonavir and Lopinavir: Protease inhibitors for HIV. Glecaprevir: Protease inhibitor for HCV. 6. Assembly and Release Inhibitors: Interfere with the assembly of new viral particles or their release from host cells. Examples: Oseltamivir and Zanamivir: Neuraminidase inhibitors for influenza. Baloxavir Marboxil: Inhibits cap-dependent endonuclease in influenza. Categories of Antiviral Drugs 1. Anti-Herpesvirus Agents: Target herpes simplex virus (HSV), varicella-zoster virus (VZV), and cytomegalovirus (CMV). Drugs: Acyclovir, Valacyclovir, Ganciclovir, Foscarnet. Nucleoside analogs that inhibit DNA polymerase. 2. Anti-Influenza Agents: Target influenza A and B viruses. Drugs: Neuraminidase inhibitors: Oseltamivir (oral), Zanamivir (inhaled). M2 inhibitors: Amantadine, Rimantadine (limited due to resistance). Categories of Antiviral Drugs 3. Anti-HIV Agents: Multiple classes targeting HIV replication: Nucleoside Reverse Transcriptase Inhibitors (NRTIs): Zidovudine, Lamivudine. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): Efavirenz, Nevirapine. Protease Inhibitors: Ritonavir, Atazanavir. Integrase Inhibitors: Dolutegravir, Raltegravir. Entry Inhibitors: Maraviroc, Enfuvirtide. Categories of Antiviral Drugs 4. Anti-Hepatitis Agents: Hepatitis B (HBV): Tenofovir, Entecavir: Target reverse transcription.Hepatitis C (HCV): Direct-acting antivirals (DAAs): Sofosbuvir, Ledipasvir, Glecaprevir. 5. Anti-SARS-CoV-2 Agents: Drugs developed during the COVID-19 pandemic: Remdesivir: RNA polymerase inhibitor. Paxlovid (Nirmatrelvir/Ritonavir): Protease inhibitor. Molnupiravir: RNA mutagenic agent. 6. Broad-Spectrum Antivirals: Effective against multiple viruses. Examples: Ribavirin (RSV, HCV), Interferons (chronic HBV, HCV). Challenges in Antiviral Therapy Resistance Development: Mutations in viral proteins can lead to reduced drug efficacy. Common in HIV, influenza, and HCV. Toxicity: Some antivirals may cause side effects such as nephrotoxicity (e.g., Foscarnet) or myelosuppression (e.g., Ganciclovir). Viral Latency: Many antivirals are ineffective against latent viruses (e.g., HIV, HSV). Cost: Newer drugs like DAAs for HCV are expensive. Limited Spectrum: Most antivirals are virus-specific, necessitating accurate diagnosis. COMMON S/E : nausea, vomiting, diarrhea, headache, dizziness, fatigue, and abdominal pain. Some antivirals, such as acyclovir, may cause nephrotoxicity and crystalluria, while others like zidovudine can lead to anemia and myelosuppression. Additionally, long-term use of antivirals may result in hepatotoxicity or peripheral neuropathy, depending on the drug. ANTI FUNGALS Antifungal agents are drugs used to treat infections caused by fungi, including yeasts, molds, and dermatophytes. They target the unique features of fungal cells, particularly ergosterol in their cell membranes and β-glucan in their cell walls, which differentiate them from human cells. ANTI FUINGALS Antifungal agents specifically target fungal components, making them selectively toxic: Disrupt Membrane Integrity: Polyenes bind ergosterol, creating pores. Inhibit Ergosterol Synthesis: Azoles and allylamines target different enzymes in the ergosterol pathway. Inhibit Cell Wall Synthesis: Echinocandins block β-glucan synthesis. Block Nucleic Acid Synthesis: Flucytosine acts as a pyrimidine analogue. Disrupt Fungal Mitosis: Griseofulvin interferes with spindle fibers. CLASSIFICATIONS 1. Polyenes Examples: Amphotericin B, Nystatin Bind to ergosterol in the fungal cell membrane, creating pores that lead to leakage of intracellular contents. Amphotericin B: Systemic fungal infections (e.g., Cryptococcosis, Histoplasmosis, Candidiasis). Nystatin: Topical treatment for oral and esophageal candidiasis. Nephrotoxicity (Amphotericin B). Infusion-related reactions (fever, chills). CLASSIFICATIONS 2. Azoles Examples: Fluconazole, Itraconazole, Voriconazole Inhibit lanosterol 14-α-demethylase, a key enzyme in ergosterol biosynthesis, leading to membrane disruption. Fluconazole: Candida infections, Cryptococcal meningitis. Voriconazole: Aspergillosis. Hepatotoxicity. QT prolongation. CLASSIFICATIONS 3. Echinocandins Examples: Caspofungin, Micafungin, Anidulafungin Mechanism: Inhibit β-glucan synthase, disrupting fungal cell wall synthesis. Invasive candidiasis. Refractory Aspergillosis. Minimal; occasional hepatotoxicity. CLASSIFICATIONS 4. Allylamines Examples: Terbinafine Inhibit squalene epoxidase, disrupting ergosterol synthesis and leading to toxic accumulation of squalene. Dermatophyte infections (e.g., Tinea corporis, Tinea pedis). Toxicities: Hepatotoxicity. Taste disturbances. CLASSIFICATIONS Pyrimidine Analogues Example: Flucytosine Converted into 5-fluorouracil within fungal cells, inhibiting DNA and RNA synthesis. Combined with Amphotericin B for Cryptococcal meningitis. Bone marrow suppression. GI upset. Adverse Effects: Monitor kidney function with Amphotericin B. Liver enzymes with Azoles and Terbinafine. Bone marrow suppression with Flucytosine. Drug Interactions: Azoles inhibit CYP450 enzymes, leading to interactions with warfarin, statins, etc. Patient-Specific Factors: Pregnancy: Terbinafine and Amphotericin B are preferred. Immunocompromised hosts: Aggressive systemic antifungal therapy is required. ANTI PARASITIC DRUGS Antiparasitic drugs are used to treat infections caused by parasites, including protozoa, helminths (worms), and ectoparasites (e.g., lice, scabies). These drugs act by targeting various biological processes in the parasites that are crucial for their survival, replication, or ability to cause disease. Mechanism of Action of Antiparasitic Drugs Disruption of Cell Membrane Integrity: Artemisinin, Praziquantel: Alter the integrity of the parasite’s membrane, leading to cellular damage. Inhibition of Folic Acid Synthesis: Pyrimethamine (used in malaria) inhibits dihydrofolate reductase, which is crucial for DNA synthesis in the parasite. Inhibition of Tubulin Formation: Albendazole, Mebendazole : Prevent polymerization of tubulin, inhibiting the parasite’s ability to absorb glucose and grow. Interference with Energy Metabolism: Ivermectin and Atovaquone: Disrupt mitochondrial function i n parasites, leading to energy depletion and death. Neurotoxic Effects: Permethrin and Malathion: Cause paralysis in ectoparasites, leading to their death. 1.1 Antiprotozoal Agents Protozoa are single-celled organisms responsible for diseases such as malaria, giardiasis, and amebiasis. Antiprotozoal drugs target various stages in the parasite’s life cycle. Mechanism of Action: ✔ Chloroquine: Interferes with heme detoxification in the malaria parasite, leading to the accumulation of toxic heme. ✔ Metronidazole: Interferes with DNA synthesis and function in protozoa. ✔ Artemisinin Derivatives (e.g., Artesunate): Disrupt parasite metabolism and damage cellular components. ✔ Atovaquone-Proguanil: Disrupts mitochondrial function in the malaria parasite, leading to energy depletion. 1.2 Antihelminthic Drugs Helminths are multicellular parasitic worms that cause diseases like ascariasis, schistosomiasis, and filariasis. Antihelminthic drugs target the metabolic pathways and structures of these worms. Mechanism of Action: ✔ Albendazole, Mebendazole: Inhibit microtubule formation, disrupting the parasite’s ability to absorb glucose, leading to its death. ✔ Ivermectin: Paralyzes and kills parasites by stimulating chloride influx through glutamate-gated chloride channels, affecting neuromuscular function. ✔ Praziquantel: Increases the permeability of the parasite’s membrane to calcium ions, causing paralysis and disintegration of the worm. 1.2 Ectoparasiticides Ectoparasiticides target parasites like lice, mites, and ticks, which infest the skin or external body surfaces.Mechanism of Action: ✔ Permethrin: Disrupts nerve cell function by inhibiting sodium ion influx through the nerve membrane, leading to paralysis. ✔ Malathion: Organophosphate that inhibits acetylcholinesterase, leading to neurotransmitter accumulation and paralysis. ✔ Lindane: Acts on the nervous system of the ectoparasites, causing their death by disrupting the central nervous system. ADVERSE EFFECTS/S/E gastrointestinal distress such as nausea, vomiting, diarrhea, and abdominal pain Central nervous system effects like headache, dizziness, and insomnia may also occur. Hematologic effects, including bone marrow suppression leading to anemia or leukopenia, are possible. Hypersensitivity reactions, ranging from rash and pruritus to severe anaphylaxis, can pose significant risks. Hepatotoxicity, marked by elevated liver enzymes and jaundice, Neurotoxicity cardiotoxicity, including QT prolongation and arrhythmia Drug-to-Drug Interactions Metronidazole: Interaction with alcohol causing a disulfiram-like reaction. Chloroquine: Increased risk of cardiotoxicity with QT-prolonging agents. Albendazole: Enhanced toxicity with cytochrome P450 inhibitors like cimetidine. Ivermectin: Increased CNS effects with sedatives or benzodiazepines. Pyrimethamine: Increased bone marrow suppression with folate antagonists. Antimalarial drugs: Interaction with anticoagulants, increasing bleeding risk. Nursing Responsibilities and Considerations for Anti-Infectives 1. Assess for allergies, especially to antibiotics like penicillin or sulfa drugs. 2. Obtain cultures before starting anti-infective therapy. 3. Monitor renal and liver function to adjust dosages if needed. 4. Administer at the correct time to maintain therapeutic levels. 5. Ensure accurate dose calculation based on weight for pediatric and elderly patients. 6. Monitor for signs of hypersensitivity, such as rash or anaphylaxis. 7. Educate the patient to complete the full course of therapy. 8. Encourage adequate hydration to support renal function. 9. Monitor for superinfections, such as oral thrush or C. difficile. 10.Check for drug interactions, especially with anticoagulants or other antibiotics.