INFECTIOUS DISEASE I: BACKGROUND & ABX BY DRUG CLASS

Common Pathogens CNS/Meningitis

Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Group B Streptococcus/E. coli (young), Listeria (young/old).

Common Pathogens Upper Respiratory

Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis.

Common Pathogens Heart/Endocarditis

Staphylococcus aureus (including MRSA), Staphylococcus epidermidis, Streptococci, Enterococci.

Common Pathogens Skin/Soft Tissue

Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Pasteurella multocida, aerobic/anaerobic gram-negative rods (in diabetes).

Common Pathogens Bone/Joint

Staphylococcus aureus, Staphylococcus epidermidis, Streptococci, Neisseria gonorrhoeae, gram-negative rods (in specific situations).

Common Pathogens Mouth

Mouth flora (Peptostreptococcus), anaerobic gram-negative rods (Prevotella, others), Viridans group streptococci.

Common Pathogens Intra-abdominal

Enteric gram-negative rods, Enterococci, Streptococci, Bacteroides species.

Common Pathogens Lower Respiratory (Community)

Streptococcus pneumoniae, Haemophilus influenzae, Atypicals (Legionella, Mycoplasma, Chlamydophila), Enteric gram-negative rods (in alcohol use disorder).

Common Pathogens Lower Respiratory (Hospital)

Staphylococcus aureus (including MRSA), Pseudomonas aeruginosa, Acinetobacter baumannii, Enteric gram-negative rods (including ESBL+, MDR), Streptococcus pneumoniae.

Common Pathogens Urinary Tract

E. coli, Proteus, Klebsiella, Staphylococcus saprophyticus, Enterococcus.

Empiric Treatment

Broad-spectrum antibiotics started before pathogen identification, guided by local resistance patterns and antibiograms.

Culture and Susceptibility Testing

Identifies the infecting organism and determines which antibiotics it is susceptible or resistant to.

Minimum Inhibitory Concentration (MIC)

The lowest concentration of an antibiotic that inhibits bacterial growth.

Gram-Positive Clusters

Staphylococcus spp. (including MSSA, MRSA).

Gram-Positive Pairs and Chains

Streptococcus pneumoniae (diplococci), Streptococcus spp., Enterococcus spp.

Gram-Negative Cocci

Neisseria spp.

Gram-Negative Rods that Colonize the Gut

Proteus mirabilis, Escherichia coli, Klebsiella spp., Serratia spp., Enterobacter cloacae, Citrobacter spp.

Gram-Negative Rods that Do Not Colonize the Gut

Pseudomonas aeruginosa, Haemophilus influenzae, Providencia spp.

Common Resistant Pathogens (Mnemonic: Kill Each And Every Strong Pathogen)

Klebsiella pneumoniae (ESBL, CRE), Escherichia coli (ESBL, CRE), Acinetobacter baumannii, Enterococcus spp. (VRE), Staphylococcus aureus (MRSA), Pseudomonas aeruginosa.

Extended-Spectrum Beta-Lactamases (ESBLs)

Enzymes that break down penicillins and most cephalosporins, requiring treatment with carbapenems or beta-lactamase inhibitor combinations.

Carbapenem-Resistant Enterobacterales (CRE)

Highly drug-resistant gram-negative organisms requiring polymyxins or ceftazidime/avibactam (Avycaz).

Antibiotic Degradation

Bacteria produce enzymes (e.g., beta-lactamases) that break down antibiotics before they can act.

Atypical Bacteria

Chlamydia spp., Legionella spp., Mycoplasma pneumoniae, Mycobacterium tuberculosis.

Synergy in Antibiotic Therapy

Using two antibiotics together for an enhanced effect (e.g., aminoglycosides and beta-lactams in infective endocarditis).

IV to PO Conversion Criteria

Patient is stable, eating, and an appropriate oral drug is available to penetrate the infection site.

What Factors Determine the Presence of an Infection?

Signs and symptoms (e.g., fever, elevated WBC, site-specific symptoms), diagnostic findings (e.g., cultures, X-rays, inflammatory markers).

Antibiotic Selection Criteria

Based on infection site, severity, risk of MDR pathogens, antibiotic characteristics (spectrum, penetration), patient factors (age, weight, renal/liver function, allergies), and treatment guidelines.

Antibiogram

A chart summarizing bacterial susceptibility data at an institution to guide empiric antibiotic selection.

Gram Stain Results

Gram-positive: Thick cell wall, stains purple/blue. Gram-negative: Thin cell wall, stains pink. Atypical organisms: Do not stain well.

Purpose of an MIC in Culture and Susceptibility Reports

Determines the minimum antibiotic concentration needed to inhibit bacterial growth.

Antibiotic Resistance Mechanisms

Intrinsic: Natural resistance (e.g., E. coli to vancomycin). Selection pressure: Eliminating susceptible bacteria allows resistant strains to thrive. Acquired resistance: Transfer of resistant genes between bacteria. Antibiotic degradation: Bacterial enzymes break down antibiotics.

Significance of Clostridioides difficile (CDI) Infection

Occurs when antibiotics disrupt gut flora, leading to overgrowth of C. difficile and toxin production, causing diarrhea and colitis.

Goal of Antimicrobial Stewardship Programs

Improve patient outcomes, reduce drug resistance, minimize adverse effects, and optimize cost-effectiveness.

Spectrum of Activity

The range of bacteria an antibiotic is effective against (e.g., broad-spectrum vs. narrow-spectrum).

Empiric vs. Definitive Therapy

Empiric: Broad-spectrum treatment before pathogen identification. Definitive: Narrow-spectrum treatment based on culture results.

Selection Pressure and Resistance

Antibiotic use kills susceptible bacteria, allowing resistant strains to proliferate (e.g., VRE emerging in patients treated with vancomycin).

Purpose of an Antibiogram

Guides empiric antibiotic selection by showing local bacterial susceptibility patterns.

Coagulase Test for Staphylococci

Staphylococcus aureus is coagulase-positive, while Staphylococcus epidermidis and other coagulase-negative Staphylococci (CoNS) are coagulase-negative.

C. difficile Infection (CDI) Risk Factors

Broad-spectrum antibiotic use (penicillins, cephalosporins, fluoroquinolones, carbapenems, clindamycin), hospitalization, advanced age, immunosuppression.

IV to PO Conversion Benefits

Reduces hospital stay, lowers costs, decreases risk of IV-related complications, improves patient comfort.

Definitive Therapy

Narrow-spectrum treatment selected based on culture results and antibiotic susceptibility testing.

Role of Normal Flora

Helps prevent pathogen colonization but can cause infections when introduced to normally sterile sites.

Bacterial Cell Wall Composition

Gram-positive bacteria have a thick peptidoglycan layer, while gram-negative bacteria have a thinner wall and an outer membrane.

Gram Stain Purpose

Differentiates bacteria based on cell wall structure to help guide empiric antibiotic selection.

Antimicrobial Stewardship Goals

Optimize antibiotic use to reduce resistance, minimize adverse effects, and improve patient outcomes.

Colonization vs. Infection

Colonization refers to bacteria present without causing disease, while infection involves tissue invasion and an immune response.

Common Sources of Infection

Respiratory tract, urinary tract, bloodstream, skin/soft tissue, intra-abdominal, and central nervous system.

Host Factors in Infection Risk

Age, immune status, comorbidities, prior antibiotic use, and presence of foreign devices (e.g., catheters, ventilators).

Biofilm Formation

Some bacteria form biofilms on medical devices, making infections more difficult to treat.

Anaerobic Bacteria Characteristics

Thrive in oxygen-poor environments, commonly found in intra-abdominal infections and deep tissue abscesses.

Multidrug-Resistant (MDR) Pathogens

Bacteria resistant to at least one agent in three or more antimicrobial classes.

Empiric Therapy for Life-Threatening Infections

Often involves broad-spectrum coverage, including gram-positive, gram-negative, and anaerobes.

Factors Affecting Antibiotic Penetration

Blood supply, tissue barriers (e.g., blood-brain barrier), and drug properties influence effectiveness at the infection site.

Hospital-Acquired Infections (HAIs)

Occur 48+ hours after hospital admission and often involve resistant organisms.

Community-Acquired Infections (CAIs)

Acquired outside of healthcare settings, often caused by less resistant pathogens.

Antibiotic De-Escalation

Switching from broad-spectrum to narrow-spectrum therapy once pathogen and susceptibility results are available.

Bactericidal vs. Bacteriostatic Antibiotics

Bactericidal: Kill bacteria (e.g., beta-lactams). Bacteriostatic: Inhibit growth (e.g., macrolides).

Nosocomial Pneumonia Pathogens

Staphylococcus aureus (including MRSA), Pseudomonas aeruginosa, Acinetobacter baumannii, enteric gram-negative rods.

Sepsis and Septic Shock

Life-threatening response to infection characterized by organ dysfunction and low blood pressure despite fluids.

Antibiotic Stewardship Strategies

Prospective audit and feedback, formulary restrictions, dose optimization, and rapid diagnostic testing to guide therapy.

Key Steps in Identifying Infection

Assess patient symptoms, obtain cultures, start empiric therapy, review microbiology results, and adjust to definitive therapy.

Normal WBC Range

4,000-11,000 cells/mm³; elevated in bacterial infections (leukocytosis), low in severe infections or immunosuppression (leukopenia).

Systemic Signs of Infection

Fever (>100.4°F), chills, elevated WBC count, tachycardia, hypotension, altered mental status (especially in severe infections).

Localized Signs of Infection

Pain, redness, swelling (skin infections); productive cough (pneumonia); dysuria, urgency (UTI); abdominal pain (intra-abdominal infection).

Interpreting Culture Results

Identify pathogen, determine antibiotic susceptibility (S = susceptible, I = intermediate, R = resistant), and de-escalate therapy accordingly.

Polymicrobial Infections

Common in intra-abdominal infections, diabetic foot infections, and aspiration pneumonia, requiring broad-spectrum coverage.

Common Sites for Bloodstream Infections (BSIs)

IV catheters, prosthetic devices, urinary tract, lungs (pneumonia), GI tract.

Risk Factors for Candidemia (Fungal Bloodstream Infection)

Broad-spectrum antibiotic use, central venous catheters, total parenteral nutrition (TPN), immunosuppression.

Bacterial Meningitis in Different Age Groups

Neonates: Group B Strep, E. coli, Listeria. Adults: Strep pneumoniae, Neisseria meningitidis.

Common Urinary Tract Infection (UTI) Symptoms

Dysuria, frequency, urgency, suprapubic pain, hematuria; fever and flank pain indicate pyelonephritis.

Key Differences Between CA-MRSA and HA-MRSA

CA-MRSA is more susceptible to oral antibiotics (e.g., TMP-SMX, doxycycline), while HA-MRSA requires IV agents (e.g., vancomycin, daptomycin).

Common Contaminants in Blood Cultures

Coagulase-negative Staphylococcus, Corynebacterium, Bacillus spp., Cutibacterium acnes (if only in one culture bottle, likely contamination).

Common Pathogens in Catheter-Associated UTIs (CAUTIs)

E. coli, Klebsiella, Pseudomonas, Enterococcus, Candida (fungal UTIs in immunocompromised patients).

Antibiotics with High Oral Bioavailability

Fluoroquinolones, linezolid, metronidazole, doxycycline, TMP-SMX; allow IV to PO conversion when appropriate.

High-Risk Factors for Hospital-Acquired Pneumonia (HAP)

Ventilator use, prolonged hospitalization, prior antibiotic exposure, immunosuppression.

Role of Inflammatory Markers in Infection

CRP and ESR can indicate inflammation/infection but are non-specific.

Why Atypical Bacteria Don't Stain on Gram Stain

Lack a traditional cell wall or have unique cell wall structures (e.g., Mycoplasma has no cell wall, Legionella has an intracellular lifestyle).

Sterile vs. Non-Sterile Body Sites for Culture Interpretation

Sterile: Blood, CSF, pleural fluid, peritoneal fluid. Non-sterile: Skin, sputum, GI tract (normal flora present).

Antibiotic Stewardship Core Principles

Avoid unnecessary antibiotic use, select the narrowest effective spectrum, optimize duration and dose, monitor patient response, prevent resistance.

Factors Leading to Recurrent Infections

Incomplete treatment, poor host immune response, resistant pathogens, presence of foreign devices (e.g., catheters, prosthetics).

Bactericidal antibiotics

Kill bacteria by disrupting cell wall, membrane, or DNA/RNA synthesis.

Bacteriostatic antibiotics

Inhibit bacterial growth by targeting protein or folic acid synthesis.

Cell wall inhibitors

Beta-lactams (penicillins, cephalosporins, carbapenems), monobactams (aztreonam), vancomycin, dalbavancin, telavancin, oritavancin.

Cell membrane inhibitors

Polymyxins, daptomycin, telavancin, oritavancin.

DNA/RNA inhibitors

Quinolones (inhibit DNA gyrase, topoisomerase IV), metronidazole, tinidazole, rifampin.

Folic acid synthesis inhibitors

Sulfonamides, trimethoprim, dapsone.

Protein synthesis inhibitors

Aminoglycosides, macrolides, tetracyclines, clindamycin, linezolid, tedizolid.

Sulfonamides mechanism of action

Inhibit folic acid synthesis by blocking dihydropteroate synthase.

Trimethoprim mechanism of action

Inhibits dihydrofolate reductase, blocking folic acid synthesis.

Beta-lactam mechanism of action

Inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs).

Monobactam (aztreonam) function

Inhibits bacterial cell wall synthesis but is structurally different from beta-lactams.

Vancomycin mechanism of action

Inhibits bacterial cell wall synthesis by binding to D-Ala-D-Ala terminal of peptidoglycan precursors.

Daptomycin mechanism of action

Binds to bacterial membranes, causing depolarization and cell death.

Polymyxins mechanism of action

Disrupt bacterial cell membrane integrity, leading to leakage of intracellular contents.

Quinolones mechanism of action

Inhibit bacterial DNA gyrase and topoisomerase IV, preventing DNA replication.

Metronidazole/tinidazole mechanism of action

Cause DNA strand breakage and inhibit nucleic acid synthesis.

Rifampin mechanism of action

Inhibits bacterial RNA polymerase, preventing RNA synthesis.

Aminoglycosides mechanism of action

Bind to 30S ribosomal subunit, causing misreading of mRNA and inhibiting protein synthesis.

Macrolides mechanism of action

Bind to 50S ribosomal subunit, inhibiting bacterial protein synthesis.

Tetracyclines mechanism of action

Bind to 30S ribosomal subunit, preventing tRNA attachment and protein synthesis.