Received: 14 June 2023 | Accepted: 27 September 2023

DOI: 10.1002/jhm.13220

REVIEW

Ten common misconceptions about antibiotic use

in the hospital

John C. Lam MD, FRCPC1 | Samuel Bourassa‐Blanchette MDCM, FRCPC2,3

1
Division of Infectious Diseases, Department of Medicine, University of California Los Angeles, Los Angeles, California, USA
2
Division of Infectious Diseases, Department of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada
3
Division of Microbiology, Department of Pathology and Laboratory Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada

Correspondence
John C. Lam, MD, FRCPC, Division of
Infectious Diseases, Department of Medicine,
911 Broxton Ave, Suite 301, Los Angeles,
CA 90024, USA.
Email: john.c.lam@ucalgary.ca
Abstract
Antimicrobials are one of the most administered medications in hospitals.
Thoughtful and rational antibiotic prescribing by clinicians are important in reducing
the adverse effects to both the host that takes the antibiotic and also the individuals
in the host's community. Principles informing antibiotic prescribing in the hospital
are commonly rooted in misconceptions. We review 10 common myths associated
with antibacterial usage in hospitalized patients and share contemporary evidence in
hopes of enhancing evidence‐informed practice in this patient care setting.

I NTR O D U C TI O N have a wide spectrum of pathogen coverage. Examples of

Antibiotics are among the most frequently used drugs in hospitals,
with more than 50% of hospitalized patients receiving antibiotics at
any given time and more than half of antibacterial prescriptions either
inappropriate or suboptimal.1,2 While ID specialists can assist with
improving antimicrobial prescribing, they are not readily available in
all inpatient medical centers. Multiple misconceptions about anti-
biotic prescribing are dogmatized.
With the growing recognition of adverse effects associated with
undeterred antibiotic usage, deliberate and informed decision‐making
pertaining to antimicrobial usage is crucial for both patients and
hospitals.3 We sought to review 10 common misconceptions of
antibacterial usage in hospitalized individuals
Broad‐spectrum antibacterials are more effective than
narrow‐spectrum antibacterials
When describing antibiotics, the terms broad and potent characterize
two different concepts. Broad‐spectrum antibiotics are those that
broad‐spectrum antibacterials include piperacillin–tazobactam and
carbapenems, which have a spectrum of activity against many
gram‐positive, gram‐negative, and anaerobic bacteria. Con-
versely, potent antibiotics are agents most efficacious in the
context of a specific microbiological syndrome in a particular
infectious focus. For example, compared to piperacillin–
tazobactam, usage of narrow‐spectrum antistaphylococcal agents
such as oxacillin and cefazolin are associated with lower mortality
and improved patient outcomes when treating methicillin‐
susceptible Staphylococcus aureus (MSSA) bacteremia.4,5 Simi-
larly, while vancomycin has a broader spectrum of activity against
staphylococcal species, its use as monotherapy in MSSA bactere-
mia is discouraged due to worse clinical outcomes when
compared with oxacillin or cefazolin.
Drug penetration is another salient consideration when
assessing antibiotic efficacy. For example, while piperacillin–
tazobactam is active against Streptococcus pneumoniae, usage of
ceftriaxone for S. pneumoniae meningitis is more efficacious given
the ability of ceftriaxone to more reliably cross the blood–brain
barrier.6

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any
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© 2023 The Authors. Journal of Hospital Medicine published by Wiley Periodicals LLC on behalf of Society of Hospital Medicine.

J. Hosp. Med. 2023;18:1123–1129. wileyonlinelibrary.com/journal/jhm | 1123

1124 | TEN COMMON MISCONCEPTIONS ABOUT ANTIBIOTIC USE IN THE HOSPITAL

Lower minimum inhibitory concentrations on TABLE 1 Antimicrobials with high oral bioavailability.14
susceptibility testing mean greater efficacy Class Antibiotic

Fluoroquinolone Levofloxacin
Minimum inhibitory concentration (MIC) values are defined as the lowest
Moxifloxacin
concentration of an antibiotic in mg/L (μg/mL) that completely inhibits
the growth of a bacterial strain under controlled conditions.7 Minimal Ciprofloxacin
inhibitory concentration determination is independent of an antimicro- Oxazolidinone Linezolid
bial's ability to penetrate and accumulate at a sufficient concentration in
Tedizolid
infected tissue to provide favorable clinical outcomes. However, the MIC
Tetracycline Doxycycline
is not the only factor that determines the efficacy of an antibiotic and
cannot be directly compared between different antibiotic classes. Minocycline
Laboratory committees, including the European Committee on Anti- Lincosamide Clindamycin
microbial Susceptibility Testing and Clinical and Laboratory Standards
Nitroimidazole Metronidazole
Institute, infer in vitro susceptibility by establishing breakpoints (also
Sulfonamide Trimethoprim‐sulfamethoxazole
known as interpretive criteria) for MICs based on data from clinical,
8,9 Macrolide Azithromycin
pharmacodynamic, and pharmacokinetic studies.
The MIC interpretative criteria (or breakpoint) is dependent on Clarithromycin
the sample site (e.g., blood, urine, knee aspirate, etc.). For example,
Rifamycin Rifampin
there are breakpoints for ciprofloxacin and doxycycline for Enter-
Triazole Fluconazole
ococcus faecalis from urine cultures but not from blood cultures.
By itself, the MIC breakpoint cannot be used to compare the Voriconazole
efficacy of antibacterials. For example, the MIC breakpoint of Isavuconazole
S. pneumoniae from cerebrospinal fluid interpreted as susceptible to
Posaconazole
penicillin and ceftriaxone is less than 0.06 and 0.5, respectively.
Itraconazole
Therefore, a MIC breakpoint for penicillin that is 0.25, even though
lower than the MIC of ceftriaxone at 0.5, would represent less
efficacious treatment than ceftriaxone for S. pneumoniae meningitis.
treatment of infections, including osteomyelitis and bacteremia.
While literature supports the usage of empiric intravenous antibiotics
Bactericidal antibiotics are more effective than for patients with suspected severe or deep‐seated infection, early
bacteriostatic antibiotics transition to oral agents may be equally efficacious and safer than
maintenance of intravenous therapies.13 The method of antimicrobial
It was traditionally believed that bactericidal agents (which kill administration is irrelevant so long as antibiotic concentrations are
bacteria) were superior to bacteriostatic agents (which prevent adequate at the site of infection.
bacterial growth). However, dichotomizing antibacterials as bacteri- Concepts of oral bioavailability and drug penetration are
cidal or bacteriostatic is an oversimplified categorization of an important considerations when selecting oral antibacterials. Oral
antibiotic's mechanism of activity.10 bioavailability refers to the fraction of orally administered drugs
Contemporary literature has not identified any meaningful differ- reaching systemic circulation and being available to exact a
ence in clinical outcomes when using bacteriostatic versus bactericidal pharmacological effect at the site of infection. Multiple antimicrobials
drugs for a variety of infections such as pneumonia, skin and soft tissue have excellent oral bioavailability and should be considered equally
infections, and intra‐abdominal infections.11 Rather, the “cidality” of a efficacious as their intravenous counterpart in patients with normal
bacteriostatic agent is dependent on the antibiotic dose, as drugs that gastrointestinal absorption (Table 1).
are deemed bacteriostatic at a determined concentration are bacteri- Drug penetration refers to the ability of an agent to achieve
cidal at a higher concentration or in combination with the host–immune therapeutic concentration at the site of infection. For example, oral
response.12 The concept of bactericidal versus bacteriostatic to select fosfomycin is not an orally bioavailable agent (<50%) but has
antibiotics is not valid. excellent penetration to prostate tissue with an evolving evidence‐
based for treating chronic bacterial prostatitis.15
Contemporary literature reviewing the administration of oral
Intravenous antibacterials are more effective than versus parenteral therapy for select cases of osteomyelitis, infective
oral antibacterials endocarditis, and bacteremia has confirmed the usage of oral
therapies to be effective if optimal doses can be clinically
For decades, it has been assumed that parenteral administration of achieved.16–18 Additionally, the usage of oral therapies obviates the
antibiotics was necessary and superior to oral administration for the risk of phlebitis, thrombosis, and line‐associated bloodstream
LAM and BOURASSA‐BLANCHETTE | 1125

infections.19 ID specialists can be helpful in guiding the timing of the
transition to oral antibacterials. The paradigm of intravenous
antibacterials being superior to oral antibiotics requires continual
challenging.
Longer courses of antibacterials lead to less relapse
of infections
Historically, a belief in prolonging antibacterial durations to prevent
relapse of infection was emphasized with the goal of preventing the
development of antimicrobial resistance. However, a major shift in
this principle is underway, emerging from the realization that many
traditional recommendations on antibiotic duration were established
with limited evidence and unchallenged since their inception.20 Many
infectious syndromes can be treated with shorter antibiotic courses,
as demonstrated by contemporary literature and reevaluation of past
evidence that challenged traditional longer courses (Table 2). Not
only do shorter courses of antibacterials reduce the selection of
bacterial resistance, but each additional day of antibiotic therapy is
3,24
associated with a 4% increase in adverse drug effects.
Serial clinical assessments are useful in optimizing duration of
therapy for infections like cellulitis and pneumonia. With evidence
demonstrating that effective cellulitis and pneumonia treatment can
constitute less than 1 week of therapy, it behooves clinicians to
scrutinize the data utilized to inform previous clinical practice and
incorporate their patient's clinical course in determining durations of
therapy.20,25
Fevers require immediate initiation of antimicrobials
The presence of an isolated fever, defined as a single temperature of
38.3°C or 38.0°C for greater than 1 h, is not pathognomonic for
infection and need not be automatically countered with empiric
antimicrobial therapy. A syndromic approach with a comprehensive
history and physical examination should be undertaken to determine
the likeliest source of infection, if any. In the hospitalized patient over
25% of individuals were found to have noninfectious entities
responsible for fever—including drug reaction, malignancy, ischemia
(e.g., pulmonary embolism, and myocardial infarction), and
procedure‐related complications (e.g., blood transfusion).26,27 Empiric
antibiotics before identification of infection in a febrile patient may
delay diagnoses. Thus, in an otherwise hemodynamically stable
individual with an isolated fever, close clinical monitoring without
empiric antibiotics is a preferred approach.
Recognition and treatment of sepsis are critical for improving
mortality and morbidity. However, establishing a diagnosis of
infection via a careful clinical assessment is more prudent than
reflexively starting antibacterials.28 The axiom of empiric antimicro-
bial initiation within 1 h for patients presenting with suspected sepsis
is drawing debate.29,30 Multiple studies demonstrate no significant
mortality benefit when administering antibiotics within 1 versus
3 h of shock recognition.31,32 While antibiotics ought not be
unnecessarily delayed or withheld in patients with systemic infection,
universal administration of antibiotics to meet a strict timeline of 1 h
in patients with a vague label of sepsis is not advisable. Rather, timely
evaluation of patients for likelihood of infection and stratification of

TABLE 2 Duration of antibiotic therapy in select infections.21–23

System Infection Population Recommended duration

Urinary tract Uncomplicated cystitis Women/adolescents Nitrofurantoin—5 d

TMP‐SMX—3 d

Complicated cystitis Men 7d

Pyelonephritis Adults Quinolones or beta‐lactams 7 d

Respiratory tract Community‐acquired pneumonia Adults 5d

Nosocomial acquired pneumonia Adults ≤8 d

Intra‐abdominal Uncomplicated appendicitis Adults Preoperative antibiotics only

Traumatic bowel perforation Adults No more than 24 h postoperatively

Gastroduodenal perforation Adults No more than 24 h postoperatively

Intra‐abdominal abscess Adults 4 d after source control

Cellulitis Uncomplicated non‐purulent or purulent cellulitis Adults 5–7 d unless hospitalized with extensive or severe
disease

Osteoarticular Acute vertebral osteomyelitis Adults 6 wk

Acute native septic arthritis Adults 2 wk for small joints after drainage
4 wk for large joints after drainage

Bacteremia Gram‐negative Enterobacterales without source Adults 7d

control concerns
1126 | TEN COMMON MISCONCEPTIONS ABOUT ANTIBIOTIC USE IN THE HOSPITAL
illness severity is arguably more critical than involuntarily initiating
antimicrobials.
An immediate clinical response to antimicrobials
confirms a diagnosis of infection
Rapid improvement in clinical syndrome within 24 h of antibiotic
administration is rarely attributable to antimicrobials, thus rendering
it unlikely that an individual's syndrome originated from an
infectious etiology. A patient's clinical response may be attributed
to concomitant therapies administered in parallel with antibiotics.
For example, a patient admitted to hospital with undifferentiated
hypoxia and tachypnea who receives antibacterials, diuretics, and
steroids and returns to baseline within 24 h of antibacterials is
unlikely to have a bacterial pneumonia that was responsible for the
original presentation.
Similarly, a lack of clinical improvement after antimicrobial
initiation does not imply antimicrobial failure. Understanding the
natural course of infection is important to determine whether a
favorable clinical response is secondary to antibacterial therapy. For
example, acute bacterial pneumonia generally require 3–4 days of
33
therapy before clinical resolution. In cases of acute pyelonephritis,
prolonged fever is not reliable in identifying patients with antibiotic‐
resistant pathogens, as fevers beyond 24 h of antibiotic administra-
tion are common in pyelonephritis.34,35 In cellulitis, cessation of
expanding erythema lags behind local inflammatory improvement.
Thus, a lack of clinical improvement after 1 day of antibacterials is not
predictive of clinical failure.36
Antibacterials can cure infections on their own
Usage of antibiotics to treat infection without addressing factors that
promote ongoing infection is not curative. For example, drainage of
pyogenic abscesses is critical in the treatment of sepsis, both for
restoration of normal physiological function, but also to enhance
antibacterial absorption into infected spaces.37 Penetration of
antibacterials into abscesses is limited and unreliable.38 Similarly,
patients with diabetes and non‐revascularizable peripheral arterial
disease who develop diabetes‐related foot infections may not have
cure of infection with antibiotics alone.39 Critically ill patients benefit
when source control procedures are undertaken within the first 12 h
of diagnosis.40
The usage of antibiotics is also limited in eradicating infections in
the context of hardware involvement. The presence of catheters,
orthopedic hardware, and vascular grafts renders infection difficult to
treat. Compared to planktonic pathogens, bacteria present within a
matrix of biofilm are less sensitive to antibiotics. Lack of oxygen
availability, impaired neutrophil oxidative killing capacity, and physical
biofilm barriers contribute to reduced antibacterial efficacy.41,42
In individuals who are immunocompromised, reducing or
eliminating the net state of immunosuppression portends a
favorable clinical course from infection. Similarly, recovery of
neutrophils in individuals with neutropenia also have a major role
in the resolution of infection.
Antimicrobials can be used to prevent nosocomial
infections
Counterintuitively, restrictive antibacterial usage can prevent infec-
tions in hospitalized patients.43 Administration of antibiotics in
hospitalized patients alters a host's microbiome and increases the
proportion of multidrug‐resistant organisms that constitute normal
flora. For example, the usage of a carbapenem for a urinary tract
infection selects for bacterial resistance in gut and lung flora.
Translocation of resistant bacteria occurs between different sites of
the body. Reducing multidrug‐resistant organism intestinal coloniza-
tion by reducing the usage of antibacterials represents an effective
way in preventing pulmonary infections from multidrug‐resistant
organisms in ill patients.44
Outside of perioperative prophylaxis, antibacterials are rarely
effective in preventing infection in hospitalized patients. For example,
prophylactic antibacterial therapy is prescribed to approximately 75%
of hospitalized patients with acute aspiration events, although no
reduction in mortality or reduced length of stays in critical care units
has been observed.45,46
Usage of antimicrobials in the outpatient setting to suppress
infection in nonoperable deep‐seated infections, including pros-
thetic joint infections, vascular graft infections, and cardiovascu-
lar implantable electronic device infections, are guided by limited
data and appear rational in select circumstances. 47 Within a
hospital environment, it is rare for patients to benefit from
prolonged antibacterial usage—and consideration of such should
be guided by ID consultants if available.
The risks of antibacterial usage are limited to patients
receiving them
Antibacterial usage and subsequent development of resistance
impact an ecosystem. Compared to a community, hospitals have a
constant influx and efflux of patients colonized with a variety of
commensal pathogens. Usage of antibacterials replaces the micro-
biome of patients with more resistant strains of normal flora.
Moreover, hospital staff can act as vectors and transmit resistant
pathogens between patients.48
The advent of vancomycin‐resistant enterococci (VRE) infec-
tions and the emergence of vancomycin‐dependent enterococcus
illustrate the concept of ecological impact from antibacterial
usage. 49 Enterococci are commensal bacteria within the gastro-
intestinal tract—and the increasing usage of vancomycin in the
latter part of the 20th century has led to increased rates of VRE,
via mutations from antibiotic selection pressures and horizontal
transmission between patients.50 As a result, outbreaks of
LAM and BOURASSA‐BLANCHETTE
FIGURE 1 Reframing 10 common misconceptions about antibiotic use in the hospital.
infections from VRE followed, affecting those who may not have
been colonized with VRE on admission as well as those who did
not receive antibacterials.51–53
Antibiotics increase the risk of specific types of infections in
patients with rooms close to antibiotic‐exposed patients even if they
are not receiving antibiotics themselves.54 In hospitalized patients,
the risk of C. difficile infection is enhanced in patients in beds
previously occupied by individuals who received antibiotics, even if
the prior habitant did not have C. difficile infection.55
Summary
Antibiotics are prescribed in nearly half of patients admitted to
hospital.56 Numerous myths regarding antibacterial prescribing
abound, with several entrenched in doctrine that require questioning.
We identify and elaborate on 10 misconceptions about antimicrobial
prescribing in hospitalized patients (Figure 1). By doing so, we intend
to highlight and promote optimal antibiotic usage to improve the
health of all hospitalized individuals—not only those requiring
antibacterials but those around them who do not.
A C KN O W L E D G M E N T S
This research did not receive any specific grant from funding agencies
in the public, commercial, or not‐for‐profit sectors.
CO NFL I CT OF INTERES T S T ATEME NT
The authors declare no conflict of interest.
D A TA A V A I L A B I L I T Y S T A T E M E N T
All authors had access to the data and a role in writing this
manuscript.
| 1127
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How to cite this article: Lam JC, Bourassa‐Blanchette S.
Ten common misconceptions about antibiotic use in the hospital.
J Hosp Med. 2023;18:1123‐1129. doi:10.1002/jhm.13220