Antibiotics, once the forefront and quintessence of modern medicine, are unfortunately progressing at a pace that has been superseded by the advent of new antibiotic resistance mechanisms poised by bacteria. Before the time of antibiotics, countless deaths occurred due to rampant infections caused by the myriad of diseases that people were often exposed to. Ancient civilizations would conjure up concoctions made from various medicinal herbs and/or invoke the power of greater deities to aid in then recovery of their affected. However, it wasn’t until 1928 that Alexander Fleming discovered penicillin adventitiously via a mold spore in a petri dish of bacteria. This was the most important milestone in the 20th century as we now officially had a surefire cure against gram-positive infections common to man. Thus, the road was paved for the exponential increase in the discovery and innovation of numerous new antibiotics of various mechanisms and classes. As part of this endeavor for a refresher course in antibiotics and their functions, I have designed this thread to encompass the topics of antibiotic classifications, antibiotic resistance, and the antibiotic usage guidelines established by the Infectious Diseases Society of America (IDSA).
To start off it is vital to know the mechanism by which antibiotics work. The primary target of antibiotics is to affect a unique characteristic of the bacteria cell that isn’t coincidentally also on the human cell; in this way, the potential of inhibiting or destroying the bacteria is maximized while also ensuring that the body isn’t harmed in that process. Usually, the most vital difference is the fact that bacteria have a cell wall that encapsulates all the necessary cell components necessary to bacteria survival. Next, the enzymes present in bacteria cells are slightly different compared to human cell enzymes, along with different ribosome sizes. Therefore, it would make sense for antibiotics to be designed to target these specific differences in cell components in order to avoid toxicity; and, as a result, antibiotics that aren’t as selective, as you’ll see later, will have unfavorable side effects to the body.
To simplify things a little bit, we will divide antibiotics into two major categories: bactericidal and bacteriostatic.
Bactericidal antibiotics impose a direct action on the bacteria by either killing or lysing the cell, resulting in complete cell destruction. To do so, they target biochemical pathways involved in cell wall assembly in order to produce a compromised cell wall with missing or altered components. Then, subsequent bacteria cell divisions will produce weaker cell walls that eventually lead to the complete failure of the cell wall to protect and uphold the integrity of the bacteria. These cells then lyse and die and can no longer replicate. Bactericidal antibiotics can then be divided further into those that utilize a concentration-dependent kill vs. those that utilize a time-dependent kill. We will talk more about this later on in the thread. These types of antibiotics are typically reserved for serious infections that need the effect of a bactericidal antibiotic in order to completely clear the infection, e.g. infections in the immunocompromised or meningitis.
Bacteriostatic antibiotics, on the other hand, do not directly kill the bacteria and instead only inhibit the bacteria from reproducing. These antibiotics are ones that you have to take for the full course of therapy, otherwise the potential for relapse will be high as the effects of bacteriostasis are reversible. These antibiotics target nucleic acid and protein synthesis, which are required in the replication process. By effectively slowing down bacterial growth, they allow the host immune system to ramp up enough to destroy the bacteria.
In this next part, I will list out the antibiotics belonging to each group.
References:
1) Calhoun C, Wermuth HR, Hall GA. Antibiotics. [Updated 2021 Jun 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from https://www.ncbi.nlm.nih.gov/books/NBK535443/
2) Ribeiro da Cunha B, Fonseca LP, Calado CRC. Antibiotic Discovery: Where Have We Come from, Where
Do We Go?. Antibiotics (Basel). 2019;8(2):45. Published 2019 Apr 24. doi:10.3390/antibiotics8020045
3) American Chemical Society International Historic Chemical Landmarks. Discovery and Development of
Penicillin. http://www.acs.org/content/acs/en/education/whatischemistry/landmarks/flemingpenicillin.html
Topical antibiotic stewardship has become an increasingly important consideration in dermatology, wound care, and pharmacy practice. While topical antibiotics such as mupirocin, clindamycin, erythromycin, and neomycin are commonly used to prevent or treat superficial skin infections, overuse and inappropriate application have contributed to the growing problem of antimicrobial resistance, delayed wound healing, allergic contact dermatitis, and unnecessary healthcare costs.
Topical antibiotics are often prescribed for conditions such as impetigo, minor wounds, acne vulgaris, and surgical prophylaxis. However, studies have shown that topical antibiotic use is frequently excessive or unnecessary, particularly for clean surgical wounds where evidence supports the use of simple non-antibiotic dressings. In acne management, the long-term use of topical clindamycin or erythromycin monotherapy has been associated with the development of Propionibacterium acnes resistance, reducing treatment efficacy and contributing to cross-resistance with systemic antibiotics.
Clinical guidelines now emphasize the importance of limiting topical antibiotic use to clearly indicated cases, using the shortest effective duration, and often recommending combination regimens (benzoyl peroxide plus topical antibiotics for acne) to minimize resistance risk. Mupirocin remains a critical agent for methicillin-resistant Staphylococcus aureus (MRSA) decolonization, particularly in preoperative settings or high-risk populations, but emerging mupirocin resistance underscores the need for judicious prescribing practices.
Pharmacists play a crucial role in promoting topical antibiotic stewardship by reviewing prescriptions for appropriateness, educating prescribers on evidence-based alternatives, and counseling patients on correct application techniques. This includes reinforcing that topical antibiotics should not be used routinely for all minor cuts or abrasions, encouraging non-antibiotic wound care when appropriate (use of petrolatum or silicone dressings), and advising patients to complete prescribed regimens without extending therapy unnecessarily.
In addition, pharmacists can assist in identifying and managing adverse reactions such as contact dermatitis related to topical antibiotics, particularly with agents like neomycin, which is a well-known sensitizer. Reporting suspected antibiotic-resistant infections and collaborating with dermatology or infectious diseases teams further supports institutional antimicrobial stewardship goals. Optimizing the use of topical antibiotics is an essential strategy to preserve their efficacy, reduce resistance, and ensure that patients receive safe, effective skin care aligned with current best practices.
James WD. Clinical practice. Acne. N Engl J Med. 2005;352(14):1463–1472. doi:10.1056/NEJMcp033487
Spellberg B, Bartlett JG, Gilbert DN. The future of antibiotics and resistance. N Engl J Med. 2013;368(4):299–302. doi:10.1056/NEJMp1210220
Barlow JD, Wiles KS, Paller AS. Current perspectives on antibiotic use in pediatric dermatology. Pediatr Dermatol. 2018;35(2):153–163. doi:10.1111/pde.13470
Patel T, Geller A. Topical antibiotic use: balancing benefits and resistance. Dermatol Clin. 2021;39(4):613–620. doi:10.1016/j.det.2021.05.005
Centers for Disease Control and Prevention (CDC). Core Elements of Hospital Antibiotic Stewardship Programs. Updated 2023. Accessed April 2025. https://www.cdc.gov/antibiotic-use/core-elements/hospital.html