ABIM Infectious Disease key terms

The lowest concentration of an antimicrobial that visibly prevents growth of a standardized bacterial inoculum under defined laboratory conditions. It is compared against achievable drug levels and breakpoints to classify an organism as susceptible, intermediate, or resistant.

The lowest antimicrobial concentration that kills at least 99.9% of the starting bacterial inoculum, determined by subculturing clear broth tubes onto drug-free agar. It distinguishes killing from mere growth inhibition and is used in select infections such as endocarditis and bacteremia.

A defined MIC or zone-diameter threshold, set by standards bodies using pharmacokinetic, pharmacodynamic, and clinical outcome data, that categorizes an isolate as susceptible, susceptible-dose-dependent, intermediate, or resistant. Breakpoints guide whether a standard dose is likely to be effective.

Laboratory methods, including broth dilution, disk diffusion, and automated or genotypic systems, that determine whether a bacterial isolate is inhibited by relevant antimicrobials. Results are interpreted against validated breakpoints to guide therapy selection.

A pharmacodynamic pattern in which bactericidal effect depends mainly on how long the free drug concentration stays above the MIC or a multiples-of-MIC threshold, rather than on peak concentration. Beta-lactams and vancomycin exemplify this pattern, favoring frequent or prolonged infusions.

A pharmacodynamic pattern in which the rate and extent of bacterial killing rise with the peak free drug concentration relative to the MIC. Aminoglycosides and daptomycin show this behavior, supporting high-dose, extended-interval regimens.

The total drug exposure over 24 hours divided by the organism's MIC, a pharmacodynamic index predicting efficacy for agents such as vancomycin, fluoroquinolones, and azoles. Target values are linked to clinical and microbiologic cure in specific infections.

Loss of apparent drug activity when a very high bacterial density is tested, often from beta-lactamase production in a subpopulation. It is clinically relevant for organisms such as Enterobacterales with inducible enzymes and can cause treatment failure despite susceptible MICs.

A plasmid-mediated enzyme that hydrolyzes penicillins, cephalosporins, and aztreonam but is inhibited by clavulanate, rendering organisms resistant to most beta-lactams except carbapenems. Detection prompts use of carbapenems or newer beta-lactam/beta-lactamase inhibitor combinations.

A cephalosporinase, often chromosomally encoded and inducible, that confers resistance to cephamycins and third-generation cephalosporins and is not inhibited by clavulanate. Derepression during therapy can select resistant subpopulations, favoring carbapenems for serious infections.

An enzyme such as KPC, NDM, VIM, IMP, or OXA-48 that hydrolyzes carbapenems and most other beta-lactams, often leaving few treatment options. Detection by phenotypic or molecular methods directs use of ceftazidime-avibactam, meropenem-vaborbactam, or cefiderocol depending on the enzyme class.

A phenotype in which bacteria are inhibited but not killed by a drug, producing a large gap between MIC and MBC without an increase in MIC. It is associated with persistent or relapsing infection and with reduced killing by bactericidal agents.

A structured community of microorganisms attached to a surface and encased in self-produced matrix, which reduces drug penetration and metabolic activity and increases resistance to antibiotics and host defenses. It underlies device-related and chronic infections such as prosthetic valve endocarditis.

Measurement of serum drug concentrations to individualize dosing for agents with narrow therapeutic windows or unpredictable pharmacokinetics, such as vancomycin, aminoglycosides, and voriconazole. Results are interpreted with timing of the level, renal function, and the relevant pharmacodynamic target.

Dose individualization for vancomycin using the 24-hour AUC relative to the MIC, targeting roughly 400 to 600 for serious MRSA infections, rather than trough-only monitoring. Bayesian or two-level approaches estimate exposure and reduce nephrotoxicity while preserving efficacy.

Administration of a large once-daily aminoglycoside dose that exploits concentration-dependent killing and a post-antibiotic effect while limiting renal and cochlear uptake. Monitoring uses a single level to estimate exposure and adjust the interval.

Persistent suppression of bacterial regrowth after drug concentrations fall below the MIC. It is prominent with aminoglycosides and fluoroquinolones and supports less frequent dosing and extended intervals.

A coordinated set of interventions, including prospective audit and feedback, formulary restriction, rapid diagnostics, and de-escalation, designed to optimize antimicrobial selection, dose, and duration. The goals are improved outcomes, reduced resistance and adverse effects, and lower cost.

Narrowing empiric antimicrobial therapy once culture and susceptibility results or clinical improvement allow, reducing spectrum and duration. It lowers resistance selection, Clostridioides difficile risk, and toxicity without compromising outcomes when guided by data.

A periodic summary of the percentage of local isolates susceptible to each tested antimicrobial, stratified by organism and specimen source. It guides empiric therapy choices and stewardship interventions while reflecting local resistance patterns.

A structured pause, typically at 48 to 72 hours after starting empiric therapy, to reassess indication, spectrum, dose, route, and duration. It prompts de-escalation or discontinuation when the original rationale no longer holds.

The planned length of an antimicrobial course, increasingly defined by evidence-based short-course regimens for conditions such as uncomplicated gram-negative bacteremia, community-acquired pneumonia, and intra-abdominal infection. Shorter courses reduce resistance and adverse effects when clinical response is adequate.

Cleaning hands with alcohol-based rub or soap and water at defined World Health Organization moments to interrupt transmission of pathogens between patients and healthcare workers. It is the single most effective healthcare-associated infection prevention measure.

Use of gloves and gown plus dedicated equipment for patients colonized or infected with epidemiologically important organisms such as MRSA, vancomycin-resistant enterococci, or carbapenemase-producing organisms. It reduces cross-transmission during the period of colonization or illness.

A primary bloodstream infection in a patient with a central venous catheter present for more than two days that is not attributable to another site. Prevention relies on insertion bundles, chlorhexidine skin antisepsis, and prompt removal of unnecessary catheters.

Toxin-mediated colitis triggered most often by antibiotic disruption of colonic flora, producing diarrhea, abdominal pain, and sometimes pseudomembranous colitis. Diagnosis requires a positive test in a patient with compatible symptoms, and treatment uses oral vancomycin or fidaxomicin.

Instillation of processed stool from a screened donor into the gastrointestinal tract to restore a diverse microbiome. It is highly effective for recurrent Clostridioides difficile infection after standard antibiotic courses fail.

Staphylococcus aureus carrying mecA or mecC, which encodes an altered penicillin-binding protein conferring resistance to nearly all beta-lactams except ceftaroline. It causes skin, bloodstream, bone, and device infections and requires vancomycin, daptomycin, or linezolid therapy.

A cyclic lipopeptide that kills gram-positive organisms by depolarizing the cell membrane in a concentration-dependent manner. It is inactivated by pulmonary surfactant and must not be used for pneumonia; rising creatine kinase requires monitoring.

Instillation of a concentrated antimicrobial solution into a catheter lumen and leaving it dwell for hours to sterilize the catheter surface. It is used as adjunctive therapy for catheter-related bloodstream infection when catheter salvage is desired.

Infection involving an implanted foreign body such as a joint prosthesis, vascular graft, or cardiac device, typically caused by biofilm-forming staphylococci. Cure often requires device removal plus prolonged pathogen-directed antimicrobial therapy.

A nucleic acid amplification method that copies a target DNA or RNA sequence exponentially to detect pathogens with high sensitivity and specificity. It enables rapid diagnosis of organisms that are slow-growing, fastidious, or present at low burden.

A single test that simultaneously detects multiple pathogen nucleic acid targets, such as respiratory viruses or gastrointestinal pathogens, from one specimen. It speeds diagnosis but requires clinical correlation because it can detect colonization or residual nucleic acid.

A multiplex PCR test performed on cerebrospinal fluid that detects common bacterial, viral, and fungal causes of central nervous system infection within hours. It complements, but does not replace, Gram stain, culture, and cell count.

Needle sampling of cerebrospinal fluid from the lumbar subarachnoid space for cell count, chemistry, Gram stain, culture, and molecular testing. Opening pressure and paired serum glucose are needed for full interpretation; coagulopathy and mass lesions are relative contraindications.

Incubation of blood in aerobic and anaerobic media to detect bacteremia or fungemia, with collection of multiple sets from separate sites to distinguish contamination from true infection. Time to positivity and organism identity guide source evaluation and therapy.

A peptide precursor that rises in systemic bacterial infection and falls with effective therapy, while remaining lower in most viral illnesses. It is used adjunctively to support antibiotic initiation or discontinuation decisions, not as a stand-alone diagnostic test.

Tests that identify pathogens or resistance determinants within hours, including molecular panels, matrix-assisted laser desorption ionization time-of-flight mass spectrometry, and rapid antigen assays. Paired with stewardship, they shorten time to optimal therapy and reduce unnecessary antibiotics.

A technique that identifies organisms from colony material by comparing protein spectral fingerprints with reference libraries within minutes. It shortens time to species identification and, combined with stewardship, accelerates appropriate therapy.