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once the forefront and quintessence of modern medicine, are unfortunately progressing at a pace that has been superseded by the advent of new antibiotic resistance mechanisms poised by bacteria.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
Skin and soft tissue infections (SSTIs) encompass a range of conditions caused by bacterial invasion of the skin, subcutaneous tissue, and muscles. Common SSTIs include cellulitis, impetigo and abscesses. These infections are primarily caused by gram-positive bacteria, such as Staphylococcus aureus (including MRSA) and Streptococcus pyogenes. A minor local skin trauma such as a cut or abrasion can be the event that triggers the event and lead to a deeper infection. “Primary SSTIs result from the invasion of otherwise healthy skin; secondary SSTIs result from infection of already-damaged skin, such as from trauma or an underlying disease. Infections are often localized but they can also spread via the blood stream or lymphatic flow” (NIH). SSTIs can range from mild infections requiring minimal intervention to life-threatening conditions necessitating aggressive treatment. They can be categorized as superficial infections, such as impetigo, carbuncles and furuncles, or infections that penetrate the subcutaneous tissue such as cellulitis. They can be purulent or non-purulent. Purulent infections like an abscess contain pus. “The severity of the infection (mild, moderate, or severe) impacts the choice of antibiotics and the route (topical, PO, or IV)” (UWorld RxPrep) A mild infection does not have systemic signs present, a moderate infection has systemic signs present. Severe infections has systemic signs along with deeper signs of infection like fluid filled blisters, skin sloughing, hypotension, or evidence organ dysfunction. During a severe infection, patients can also be immunocompromised or have failed oral antibiotics with incision and drainage for purulent infections. Impetigo is common in children and spreads quickly. It presents as a blister like rash that may be painful or itchy and found anywhere on the skin, typically around the nose, mouth, hands, and arms. The pustules rupture and a thick yellowish clear fluid dries up and forms honey colored crusts around the area. It can be treated with a local antibiotic like mupirocin if the lesion are limited and localized. For more numerous and extensive lesions, it can be treated with cephalexin 250-500 mg by mouth four times a day. Some other measures that can be taken are using a warm wet compress to help remove dried crusts. Folliculitis is a superficial infection of the hair follicles and it looks like red pimples. Furuncles are purulent infections of the hair follicles and carbuncles are a group of infected carbuncles. These may only require warm compresses to reduce inflammation and help with drainage. Incision and drainage is what is recommended for large furuncles. Antibiotics like SMX/TMP and doxycycline may be used. Cellulitis is a diffuse bacterial infection of the dermis and subcutaneous tissues characterized by redness, warmth, swelling, and pain. It often results from skin breaches, such as cuts or ulcers. Treatment involves antibiotics like cephalexin. Clindamycin or dicloxacillin for can also be used for cellulitis. Abscesses are localized infections involving pus collection. They often require incision and drainage, and antibiotics can also be used. The antibiotic used should cover MSSA and MRSA, so SMX/TMP and doxycycline would be appropriate options, but if cultures show MSSA, cephalexin should be used. Proper wound care, hygiene, and timely medical attention can prevent SSTIs. Early recognition and treatment are vital in reducing complications and ensuring recovery.
UWorld RxPrep NAPLEX Review 2025 Chapter 22 Infectious Diseases II Page 351
www.ncbi.nlm.nihgov/books/NBK545311/