Antimicrobial Therapy

Basic Principles of Antimicrobial Therapy

• Routes of medication administration include oral, sublingual, IV, IV push, IM, and transdermal.
• Medication transport varies depending on the route of administration.
• The liver metabolizes most medications, and they are excreted in the urine.
• Nurses should monitor liver and kidney function due to medication metabolism and excretion.
• Some antibiotics have higher risks and can accumulate more than others and you should look at lab results to see this
• Antibiotics treat bacterial infections, not viral infections.
• Hospitals administer 190 million doses of oral antibiotics daily.
• Antibiotics maybe be given inappropriately. For example, when patients do not have an infection.
• When patients are treated with antibiotics, they may develop antibiotic resistance.
• Alexander Fleming won the Nobel Prize for discovering the first antibiotics.
• By the 1930s and 1940s modern antimicrobials were available.
• Modern antimicrobials have significantly reduced morbidity and mortality from infections.
• Before antimicrobials, people would die from infections.

Antibiotics

• An antibiotic is a chemical that harms other microbes.
• Antibiotics are often created in a lab and prescribed to patients for a bacterial infection.
• Culture and sensitivity tests identify bacteria and effective antibiotics.
• An antimicrobial agent is any agent that suppresses or kills microorganisms.
• Antimicrobial agents kill bacteria completely or inhibit reproduction.
• Selective toxicity must be calculated based on weight and duration, considering liver and kidney toxicity.
• Too much medication can cause toxicity to the body and there are differences in the cellular chemistry of mammals and microbes
• Toxic antimicrobials must be harmless to the host.
• Antimicrobial drugs are classified by susceptible organism or mechanism of action.
• Culture and sensitivity tests determine if an antibiotic will kill the bacteria.
• Antibiotics work through a specific mechanism of action and depend on the specific area of the cell they target.
• Bacteria have membranes, cytoplasm, ribosomes, RNA, and DNA.
• Gram-positive and gram-negative bacteria differ in their cell wall structure.
• Because of a thinner wall and an outer layer (membrane), Gram-negative bacteria are more susceptible to antibiotics
• Because of a thicker wall, Gram-positive bacteria are more difficult to penetrate, so antibiotics depend on the cell structure.

Bactericidal vs Bacteriostatic

• Bactericidal drugs directly kill bacteria at clinically achievable concentrations.
• Bactericidal drugs kill bacteria by breaking the cell wall or inhibiting enzyme replication.
• Higher doses of bacteriocidal drugs become more batericidal.
• Bacteriostatic drugs slow bacterial growth but do not cause cell death.
• Bacteriostatic drugs slow replication, subsiding the infection but do not kill the bacteria simultaneously.

Acquired and Microbial Drug Resistance

• Organisms develop resistance over time.
• Organisms may initially respond well to a drug but become less susceptible over time.
• Antibiotic resistance can happen if patients do not finish their antibiotic prescription.
• Bacteria that survive can mutate, rendering the medication ineffective in the future.
• Antibiotics for viral infections also contribute to resistance.
• Microbial drug resistance can be found with organisms like Enterococcus faecium, Staphylococcus aureus, Enterobacter species, Klebsiella species, Pseudomonas aeruginosa, Acinetobacter baumannii, and Clostridium difficile can develop microbial drug resistance.
• MRSA, VRE, and methicillin are common drug resistances.

Microbial Mechanisms of Drug Resistance

• Decrease the concentration of a drug at its site of action.
• Inactivate a drug by creating an antagonist on the site.
• Alter the structure of drug target molecules through mutation.
• Acquired resistance mechanisms include spontaneous mutation.
• These are random changes in a microbe's DNA/RNA that lead to resistance to one drug.
• Conjugation transfers extrachromosomal DNA from one bacterium to another.
• Gram-negative bacteria is has more issues drug resistance because:
  • One of the bacteria that have more issues with drug resistance
  • The wall is thinner and it's easier for the antibiotic to cross the membrane
  • it is easier for that rna and dna to mutate
• When they do culture, they find that the bacterial have resistance to all the antibiotics
• Multiple drug resistance narrows the treatment options for providers.
• Extensive antimicrobial resistance increases mortality rates.
• Antibiotics are not prescribed for viral infections like COVID unless there is a superinfection.

Antibiotic Use and Drug-Resistant Microbe Emergence

• How antibiotic use promotes resistance by creating favorable conditions for resistant microbes.
• Broad-spectrum antibiotics facilitate the emergence of resistance.
• More antibiotic use leads to faster emergence of drug-resistant organisms.
• Nosocomial infections (Healthcare-associated infections, HAI) are acquired in the hospital and spread to others.
• The number one sinner is the health care professions because Infection that is acquired in the hospital, they have an infection then they spread it to the others. Housekeepers/providers are the sinners.
• Superinfections are new infections appearing during treatment for a primary infection and they are often difficult to treat because they are drug-resistant.

Delaying Drug Resistance

• Promote adherence to appropriate prescribing guidelines, including education and discharge instructions with assessment of literacy.
• Patients on antimicrobial therapy should understand the importance of completing the course and potential side effects.
  • Educate them to complete the course of antibiotics, and educate them on side effects, some side effects cause diarrhea because they kill the healthy normal flora in the gut
• Explain to patients to contact the provider when they experience side effects and not unilaterally stop the medications on their own.
• Reduce antibiotic demand among healthy adults and parents of young children.
• Emphasize adherence to prescribed antibiotic regimens.

Public Health Action Plan to Combat Antimicrobial Resistance

• More drug-resistant antibiotics become a public hazard and a risk to the whole community.
• Any communicable bacterial infection is reported to the Department of Health.
• An increased numbers triggers prompt intervention.
• Public Health Areas
• Focus Area I: Surveillance
  • Focus Area II: Prevention and Control (washing hands, mode of transmission and wearing masks).
  • Focus Area III: Research (what contributes to the spread and on the bacteria, what medications, treatment, prevention, vaccines,)
  • Focus Area IV: Product Development (case study, clinical trials, and treating volunteers to develop safe medications)

Selection of Antibiotics

• Identify the infecting organism for drug suseptibility
  • Culture and sensitivity tests will help with this
  • If treatment is ineffective, re-evaluate.
  • Consider empiric treatment based on symptoms while awaiting culture results.
• Drug sensitivity of organism
• Host factors must be taken into account for drug selection
  • Consider patient resistance and absorption.
  • Liver and kidney function must be assessed to avoid increased damage due to excretion deficiencies.
• Consider kidney failure needs, adjusted dose.
• Consider fat content for drug solubility.
• Allergy considerations determine drug.
  • Penicillin is typically used to treat strep, but an alternative must be found for those with a penicillin allergy.
  • Ask about reactions and monitor for any effects.
  • Double-check for allergies, especially for first-time prescriptions.
• Inability to penetrate site of infection include not being able to penetrate the Brain
• Empiric therapy involves antibiotic treatment before identifying the causative organism.
• Base selection on clinical evaluation and knowledge of likely microbes if you suspect the patient has an infection, you may provide therapy before the culture results comes back, and change once the culture results are back.

Identifying Infectious Organisms and Host Factors

• Match the drug with the bug through a gram-stained preparation to determine drug susceptibility via disk-diffusion test, serial dilution, and gradient diffusion. Host factors include the following:
• Host defenses
• Site of infection
• Previous allergic reactions
• Genetic factors
• Dosage size and duration depend on transporting the medication to the site and the best route of administration.
• Systemic infections may require topical and oral medication.
• Antibiotics must be present at the site of infection for a sufficient length of time.
• Do not discontinue antibiotics prematurely.
• Teach patients to complete the course of antibiotics.
• Antibiotic combinations can enhance medication efficacy.
• Some medications work better together, like amoxicillin and clavulanate but not all, you must evaluate.
• These additives can kill bacteria and inhibit the reproduction of the calborate. Indications: Mixed infections, prevention of resistance, decreased toxicity, enhanced bacterial action
• Potential Disadvantages exist with combinations
• Prophylactic antimicrobials prevent infections rather than treating the infection:
  • Surgery
  • Bacterial endocarditis
  • Neutropenia
  • Other indications

Misuses and Monitoring of Antimicrobial Therapy

• Attempted treatment of viral infections
• Treatment of fever of unknown origin
• Fever is the body's defense with cardinal signs: redness, swelling, pain, and heat, as well a systemic response to an inflammation,
• There are various WBCs that help fight infection.
• Improper dosage - The amount, some med are given weight based or the length of treatment, how long do we need to comp,ete the treatment to completely eradicate the bacteria
• Treatment in the absence of adequate bacteriologic information
• Omission of surgical drainage
• WBCs are removed through drainage.

Monitoring - Antimicrobial Therapy

• Monitor clinical responses and laboratory results.
• Severity of infection should increase monitoring frequency.
• Clinical indicators of success: Reduced fever and resolution of signs/symptoms related to the affected organ
• Serum drug levels for toxicity:
  • Low levels to prevent harm to kidneys or liver.
  • The peak depends on route of medication, 15-30 minutes for IV, and is what level the medication is the highest number
  • Through is especially when the patient has ototoxic and administers for 2 hours, start at 8 am and finishes at 10 am within the peak.

Penicillins

• Penicillins kill bacteria by trying to penetrate the cell wall.
• Active against a variety of bacteria.
• Have low direct toxicity.
• Cause an allergic reaction.
• ask before hand, especially for the first time.
• A higher risk of allergy reaction (ask patient for allergies)
• Immediate or delayed onset can happen
• Clinical Manifestation: Can complain about skin rash,
• s/s of anaphylaxis reaction:
  • swelling, shortness of breath due to throat closing from the swelling, wheezing (an abnormal breath sound caused by narrowing of the bronchi)-> is an medical emergency (pt can't breathe NEED EPI (epinephrine injector))

About Penicillin

• It has a beta-lactam ring structure.
• The Beta-lactam family includes cephalosporins, aztreonam, imipenem, meropenem, and ertapenem.
• Weakens bacterial cell wall -> excessive water intake -> rupture. Active and Bactericidal only against bacteria undergoing growth and division.
• It has Layers: Weak cell well but a thick outer structure outside the cell well. Then another one
• Bacterial resistance happens when there is inability of penicillins to reach their target and Inactivation of penicillins by bacterial enzymes. Mechanism:
• Three factors, the inability of penicillins to reach their targets, inactivation of penicillins by bacterial enzymes, and production of penicillin-binding proteins (PBPs) that have a low affinity for penicillins.
• Staphylococcus aureus was introduced in the 1940s with penicillin.
• MRSA - developed this ability by acquiring genes that code for low-affinity PBPs from other bateria

Cell Envelope

1. Gram-negative cell envelope - Three layers - Thin cell wall and an additional outer membrane that is difficult to penetrate
2. Gram-positive cell envelope
   • Only two layers
   • Relatively thick cell wall that is easily penetrated

• Penicillinases: Beta-lactamases, which are enzymes that render pencillin ineffective.
• Bacteria produce various enzymes specific for penicillins and other beta-lactam antibiotics.

Types of Penicillin

• Penicillin Classification -Narrow-spectrum penicillins -Specific bactera that they ever (e.g if they have strep, it kill strep, coverage is not so wide) but it they have two bacteria, the will not kill both - Penicillinase sensitive -Narrow-spectrum penicillins - Penicillinase resistant - Broad-spectrum pencillins -Extended-spectrum penicillins
• Penicillin G (Benzylpenicillin) - Bactericidal to numerous gram-positive and some gram-negative organisms - Adverse effects -Least toxic of all antibotics - We think about liver, kidney, and ears, when we talk about toxicity - Penicillins are the most common cause of drug allergy

Penicillin Allergy

• Development of penicillin allergy -Skin tests for penicillin allergy - Management of patients with a history of penicillin allergy Assess for pencillin allergy in each patient who will be receiving penicillin
  • If History of Mild Reaction, consider cephalosporin (next drug of choice, if pt is allergic to pencillin) -if history of anaphylaxis, avoid administration of penicillin or cephalosporins
• Types
  • Immediate (reaction in 2 to 30 minutes) -Accelerated (reaction in 1 to 72 hours) -Delayed (reaction takes days or weeks to develop) -Anaphlaxis
    • Laryngeal edema
    • bronchoconstriction (bronchospasm -> wheezing) - Severe hypotension
• Treatment Options - Ephinephrine - If PT no response, incubate them - respiratory support Prevention
  • Skin testing ESP for Penicillin G Drug Interactions
• Antibiotics, such as Aminoglycosides, Gentamycin, Bacteriostatic antibiotics
• Probenecid, which is not used as much anymore but is used for treat uric acid (gout).

Resistent Penicillins & Combination

• Penicillinase -Resistent Penicillins: -Available -Nafcillin -Oxacillin - Dicloxacillin Broad Spectrum Penicillins
• --broad-spectrum penicillins (aminopencillins)
  • they can be used IV (mostly PO) -Ampicillins -Amoxacilin -Adverse effects ( the most adverse side effect) -Rash -Dirrhea Ectendeds- Spectrum Penicilinns (Stay longer- longer half life) -Antipseudomonal pencilins - Piperacillinn -Broad-spectrumm, but pencilinase sensative -Effective against organisms susceptible to the aminopencillins plus Pseudomonas aeruginosa Enterobacter species, Proteus (insole.
• Penicillin Combinations

Cephalosporins

• Cephalosporins (similar to penicillin!)
• Most widely used group of antibodies especially been out patient world.
• Beta-lactam Antibiotics
• Similar to penicillin structure
• both work by destroying cell wall Bactericidal that kills the bacteria driectly, it doest inhibit growth on it.
• Dose Related
• Usually given arentally
• Penicillin and cephalosporins both destroy cellular walls, both beat-lacks, low toxicity
• Differences: lest tendency to allergies ( when a pt. has penciling allergies, you would give this medications.
• low toxicity
• Mechanism of action: (almst the same as pencils, break all wall), Bind to pencilled-binding proteins (BP’s) disrupt cell wall and cause well lysis

Resistance

• Most effective against cells undergoing active growth and division Resistamce -Beta- lactamases -First generation( First one on the marketing Destroyers -Second Generation less Sensitive -The 1st and 2nd GENERATION MOST
• Therid- Fourth- antFifth GEN agents more resistant than first second GENERATION agent Classification of cephalopoings I NEED TO KNOW).
• First generation
• Cephalexi
• Second Generation
• Cedfoxiti
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• Cerotaxime
• Fort Genet
• Cedepme
• Ceddercoi
• Fifth GEERATHAN -Cefaraine

Drug Interaction Cephaloposins

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Carbapenems

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Vancomycins

• The action of vancomycin inbibits the ceel wall Synethesis

Severe infections onl -The us of vancomycin on these severe infections will kill the MSRA.

Adverese & Monobactam

• Adverse effects include:

• Ototoxicity -Red man syndrome (a common side effect)

• Problems in the Ear,

• Vancomycin will react and have interations.

• Monobactam: Aztreonam also binds to PBP3. - narrow antimicrobial spectrum -only a gram-negative bacteria has to be given. - effects similr to other bela-lactam antibiotics

Fosfomycin

• Approved for single-dose therapy of uncomplicated UTI caused from escherchia coli or enterococcu faecalis. It inhibits the synthesis of peptidoglycan polymer strands that compose the cell wall. The side effects include diarrhea, headache, vaginititis, nasueaa.

Tatracyclines

• Tetracyclines are inhibitors thag are static and helps proteion synthesis -Used for bacterial infecitons

Tetracyclines

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• Summary of major Precaution
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Macrolides

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• Liner zolid

Linezolid Class & Adverse Effects

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Aminoglycosides

AMinoglycocides

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Sulfanomides

• broad spectrum antibotics, have colosely related mechanisms and surpress bacterial growth by inhibiting folic acid.
• They are Also Bacteriostatic.
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Explore the basic principles of antimicrobial therapy, including medication administration routes, metabolism, and excretion. Learn about the importance of monitoring liver and kidney function, understanding antibiotic resistance, and the history of antibiotics from Alexander Fleming's discovery to modern antimicrobials.