The field of infectious diseases is fraught with ideas that drive our daily clinical decision making yet lack a credible scientific basis. We need rational and critical thinking to overcome these misconceptions to optimize patient outcomes.

Myth 1: Bactericidal antibiotics are better than bacteriostatic antibiotics

A commonly taught principle is that bactericidal antibiotics kill bacteria, while bacteriostatic agents inhibit the growth of bacteria. This implies that bactericidal antibiotics are more effective than their bacteriostatic counterparts and might lead clinicians to intuitively and preferentially choose bactericidal options. It is important to understand two definitions. The minimum inhibitory concentration (MIC) is the concentration of antibiotic needed to inhibit visible bacterial growth at 24 hours, while the minimum bactericidal concentration (MBC) is the concentration of antibiotic that reduces the bacterial inoculum by one-thousand-fold. A drug is considered bactericidal if the ratio of MBC to MIC is less than or equal to 4, while a ratio greater than 4 characterizes a bacteriostatic agent.[1] In other words, both bactericidal and bacteriostatic antibiotics kill bacteria, but bacteriostatic antibiotics require higher concentrations relative to their MIC to do so compared with bactericidal agents. Moreover, a drug that is bactericidal against one pathogen might be bacteriostatic against another. For example, linezolid is bacteriostatic against staphylococci but is bactericidal against streptococci.[2] A systematic review found no significant difference in efficacy between bactericidal and bacteriostatic antibiotics for treatment of skin and soft tissue infections, pneumonia, intra-abdominal infections, bacteremia, and typhoid fever.[1] In fact, several studies have demonstrated that linezolid (bacteriostatic) was superior to vancomycin (bactericidal) in treating staphylococcal infections.[1]

Myth 2: A positive response to antibiotics confirms the presence of an infection

An improvement in the patient’s clinical status is often attributed to the effect of antibiotics, which implies an infection is being treated. While this may be true, it is important not to overlook concomitant therapies that might affect the clinical response, including anti-inflammatories, IV fluids, and supplemental oxygen.[3] Additionally, some antibiotics, such as azithromycin, possess immunomodulatory properties that can attenuate the immune reaction, leading to a positive response in a patient with a noninfectious inflammatory condition.[4] Conversely, a perceived lack of response to antibiotic does not necessarily indicate treatment failure. It is important to understand the natural course of the infection to determine when a clinical response is expected. For example, in the treatment of cellulitis, symptoms and signs of inflammation can initially worsen before they get better, and it can take up to 3 days to see any improvement.[5]

Myth 3: IV antibiotics are better than oral antibiotics

There is no evidence to suggest that IV administration of antibiotics is more effective than antibiotics taken orally. In fact, numerous RCTs have demonstrated the noninferiority of oral antibiotics compared with IV antibiotics for many types of infections, including infective endocarditis, osteoarticular infections, bacteremia, urinary tract infections, cellulitis, intra-abdominal infections, and pneumonia.[6] In some studies, oral therapy was more effective than IV treatment. IV antibiotics are often overused in situations where oral therapy is appropriate. For example, an audit of 100 outpatient IV prescriptions from the emergency department at a single hospital identified that 59% of IV treatments could have been avoided.[7] IV administration carries many disadvantages, including IV-line complications, increased staff workload, reduced patient convenience and mobility, increased costs, delayed hospital discharge, and a higher carbon footprint.[6] Oral therapy should be used if there is a safe and effective oral option, there is no concern regarding ingestion or absorption of oral medications, clinical stability has been achieved, there is no source control problem that requires intervention, and there is no psychosocial reason to prefer IV therapy. Reserve IV therapy for critically ill patients and situations where oral administration is not feasible or is not supported by evidence.[6]

Myth 4: Longer courses of antibiotics are better than shorter courses

Many RCTs have shown that shorter courses of antibiotic are just as effective as longer courses for common infections.[8] To illustrate a few examples, a recent RCT demonstrated that 3 days is noninferior to 8 days for the treatment of community-acquired pneumonia in adult inpatients who have reached clinical stability,[9] a 2025 systematic review and meta-analysis of 4 RCTs showed that 7 days of antibiotic is just as effective as 14 days for uncomplicated gram-negative bacteremia,[10] and another RCT of adult males with afebrile urinary tract infections concluded that 7 days of treatment is no worse than 14 days.[11] It was previously thought that longer courses of treatment were needed to reduce the emergence of antibiotic resistance and prevent infection relapse. In fact, the longer that microbes are exposed to antibiotics, the greater the selective pressure is for drug resistance. Some advantages of shorter treatment durations are decreased drug resistance and side effects, lower costs, reduced environmental impact, and diminished risk of Clostridioides difficile colitis.[8] Local guidelines, such as those from the Fraser Health Authority, already promote shorter durations over longer durations for infections such as pneumonia, cellulitis, and urinary tract infections.[12]

Myth 5: Fever demands immediate initiation of antibiotics

A febrile patient presenting to the emergency department or a hospitalized patient who develops a fever will generally receive a workup for an infection. It is common for empiric antibiotics to be started before an infectious diagnosis is confirmed.[13] Fever is not specific for a bacterial infection and can be caused by viral infections, thromboembolic disease, autoimmune conditions, and medications.[3] Initiating antibiotics prematurely can be harmful when there is no actual infection or by delaying the diagnosis of a true infection. It is reasonable to withhold antibiotics in an otherwise stable patient with fever while working through the diagnostic process. Likewise, a patient who remains febrile or develops a new fever while receiving antibiotic therapy for a suspected or confirmed infection does not automatically require an escalation of antimicrobial treatment. A careful assessment should be made considering the natural history of the illness, searching for a potential source control problem, and evaluating for noninfectious causes of fever. On the other hand, in an unstable or septic patient, prompt initiation of appropriate antibiotics is critical and must not be deferred until further investigations are obtained.[3,13]

Myth 6: Broad-spectrum antibiotics are better than narrow-spectrum antibiotics

While broad-spectrum antibiotics cover a wide range of bacteria, they are not intrinsically more effective or safer than narrow-spectrum antibiotics. Broad-spectrum agents are recommended for the treatment of sepsis, multi-drug-resistant pathogens, and polymicrobial infections, but they can increase the risk of adverse effects if used inappropriately.[14] In methicillin-sensitive Staphylococcus aureus bacteremia, for example, the use of narrow-spectrum antibiotics such as cloxacillin is associated with lower mortality compared with the use of broad-spectrum beta-lactams.[15] The inappropriate use of broad-spectrum antimicrobials can severely deplete the patient’s natural protective microbiome, increase the risk of acquiring C. difficile colitis, and promote the development of multi-drug-resistant pathogens.[16] The efficacy of a drug depends not only on how many bacteria it can kill, but also on its ability to penetrate the site of infection, barrier to resistance, and potency.[3] Rational prescribing involves selecting the narrowest agent with a good safety profile to target the most likely pathogen(s) implicated in the infection.

Myth 7: Antibiotics are always the most important treatment for infections

Undoubtedly, antibiotics have dramatically reduced mortality for common infections. Antibacterials alone are usually curative for simple infections like cellulitis, pneumonia, and pyelonephritis. However, for more complex diseases, such as diabetic foot infections, a multiprong approach is required involving antibiotics, wound care, glycemic optimization, offloading, and vascular assessment.[17] Rarely is pharmacologic therapy alone sufficient to fully cure the problem. Aggressive antibiotic therapy is not a proper substitute for other more important interventions, such as surgical debridement of chronic osteomyelitis or drainage of an abscess. Most antibiotics do not work against bacteria in biofilms of chronic infections and have limited penetration and activity in the hostile environment of abscesses.[3]

Myth 8: Antibiotics are harmless

Telephone interviews with adult patients and parents revealed that antibiotic benefits are often overestimated and harms are often minimized, highlighting a tendency to prioritize instant gratification.[18] Antibiotics can cause many side effects, such as gastrointestinal upset, acute kidney injury, cytopenia, and hepatitis.[19] Excess use drives antibiotic resistance on individual and population levels. Inappropriate prescriptions also increase costs and pollute the environment. An underrecognized and unmeasurable effect is the negative impact of antibiotic use on the human microbiome, which serves an important role in metabolism, immunity, gut health, and psychological well-being.[20] Antibiotic use is associated with an increased risk of colon cancer, atopic diseases, and metabolic disorders.[20,21]

Myth 9: A penicillin allergy is a low priority

Penicillin allergy is the most commonly reported drug allergy, with up to 10% of the population carrying this label. However, 90% of these patients are judged not to have a true penicillin allergy after careful assessment and/or allergy testing.[22] In patients who have a confirmed immediate IgE-mediated (type 1) hypersensitivity reaction to penicillin, 80% of them outgrow it after 10 years of avoidance.[23] It is common for penicillin-allergic patients to receive antibiotics that are broader spectrum, less effective, more expensive, and more toxic.[22] Consequently, these patients are at higher risk of worse outcomes. A patient with a penicillin allergy label who has an infection for which beta-lactam antibiotics are the drug of choice should have their allergy status reviewed. Penicillin allergy delabeling is an important initiative of antimicrobial stewardship. Various tool kits and algorithms have been deployed to successfully delabel patients by obtaining a thorough allergy history, performing a direct oral challenge, or referring to an allergist for skin testing followed by oral challenge.[24]

Myth 10: A positive microbiological test confirms the presence of an infection

The diagnosis of infections is often complex, requiring clinical, biochemical, microbiological, and/or radiographic information. Microbiological testing is critical for identifying the causative pathogen but suffers from limitations. The most common tests are microscopy, culture, serology, nucleic acid amplification (NAAT), and histopathology.[25] A common misconception is that a positive test confirms the presence of an infection. For example, clinicians often misinterpret a positive urine culture as evidence of a urinary tract infection in the absence of relevant symptoms.[26] From a microbiological perspective, an infection occurs when a microorganism invades, destroys, and multiplies in host cells. The absolute method to diagnose an infection is a tissue biopsy for histopathology. However, the vast majority of infections are diagnosed without such an invasive procedure, as that would be impractical and resource intensive. The current diagnostic tools inform us if a pathogen or its components are present at a specific body site. Microscopy can reveal the presence of microbes in body fluids and tissues but cannot differentiate living from dead organisms. Microbial cultures can identify the presence of viable organisms in sterile and nonsterile sites but cannot prove infection. Serology detects antibodies against microbial antigens, but it might not be able to accurately distinguish between active and resolved infection. NAAT looks for microbial DNA but is unable to determine the viability of the organism.[25] These tests are merely pieces of the diagnostic puzzle that must be interpreted in the right clinical context. They alone cannot diagnose an infection—it is the clinician who does.

Conclusions

Myths are common drivers of decision making in the diagnosis and management of infections. They prevail because outdated information is left unchallenged or a concept that intuitively makes sense but is factually incorrect is perpetuated by many over the course of time. As new evidence emerges, it is incumbent upon clinicians to question and update the status quo to advance medicine for the betterment of our patients.

Competing interests

None declared.

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[11]

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License [11].

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Dr Wong is a clinical assistant professor in the Division of Infectious Diseases, Department of Medicine, University of British Columbia, and an infectious diseases consultant at Royal Columbian Hospital and Eagle Ridge Hospital.

Corresponding author: Dr Davie Wong, davie.wong@fraserhealth.ca [37].