‫‪ANTIBIOTICS‬‬

‫‪:‬اعداد‬

‫الصيدالنيه رغد عارف‬

 Definition
• An antibiotic is a type of antimicrobial substance active against
bacteria. It is the most important type of antibacterial agent for
fighting bacterial infections, and antibiotic medications are widely
used in the treatment and prevention of such infections.[1][2] They may
either kill or inhibit the growth of bacteria. A limited number of
antibiotics also possess antiprotozoal activity.[3][4] Antibiotics are not
effective against viruses such as the common cold or influenza;[5]
drugs which inhibit viruses are termed antiviral drugs or antivirals
rather than antibiotics.
 ANTIBIOTIC FAMILIES

•Penicillins - for example, phenoxymethylpenicillin, flucloxacillin and amoxicillin.

•Cephalosporins - for example, cefaclor, cefadroxil and cefalexin.
•Tetracyclines - for example, tetracycline, doxycycline and lymecycline.
•Aminoglycosides - for example, gentamicin and tobramycin.
•Macrolides - for example, erythromycin, azithromycin and clarithromycin.
•Clindamycin.
•Sulfonamides and trimethoprim - for example, co-trimoxazole.
•Metronidazole and tinidazole. Nitrofurantoin - used for urinary infections
•Quinolones - for example, ciprofloxacin, levofloxacin and norfloxacin.
ANTIBIOTIC MISUSE
• The first rule of antibiotics is to try not to use them, and the second
rule is try not to use too many of them."[92] Inappropriate antibiotic
treatment and overuse of antibiotics have contributed to the
emergence of antibiotic-resistant bacteria. Self-prescribing of
antibiotics is an example of misuse.[93] Many antibiotics are frequently
prescribed to treat symptoms or diseases that do not respond to
antibiotics or that are likely to resolve without treatment. Also,
incorrect or suboptimal antibiotics are prescribed for certain bacterial
infections.[38][93] The overuse of antibiotics, like penicillin and
erythromycin, has been associated with emerging antibiotic
resistance since the 1950s.[
Reducing the selection pressure for
antibiotic resistance
• In addition to developing new antibacterial treatments, it is important
to reduce the selection pressure for the emergence and spread of
antibiotic resistance. Strategies to accomplish this include well-
established infection control measures such as infrastructure
improvement (e.g. less crowded housing),[188][189] better sanitation (e.g.
safe drinking water and food)[190][191] and vaccine development,[158]
other approaches such as antibiotic stewardship,[192][193] and
experimental approaches such as the use of prebiotics and probiotics
to prevent infection.[194][195][196][197]
RESISTANCE
• Bacteria as a group or species are not necessarily uniformly susceptible or resistant to any particular
antimicrobial agent. Levels of resistance may vary greatly within related bacterial groups. Susceptibility and
resistance are usually measured as a function of minimum inhibitory concentration (MIC), the minimal
concentration of drug that will inhibit growth of the bacteria. The susceptibility is actually a range of the
average MICs for any given drug across the same bacterial species. If that average MIC for a species is in the
resistant part of the range, the species is considered to have intrinsic resistance to that drug. Bacteria may
also acquire resistance genes from other related organisms, and the level of resistance will vary depending
on the species and the genes acquired [19],[20].
• 3.1. Natural resistance
• Natural resistance may be intrinsic (always expressed in the species), or induced (the genes are naturally
occurring in the bacteria, but are only expressed to resistance levels after exposure to an antibiotic). Intrinsic
resistance may be defined as a trait that is shared universally within a bacterial species, is independent of
previous antibiotic exposure, and not related to horizontal gene transfer [20],[21]. The most common
bacterial mechanisms involved in intrinsic resistance are reduced permeability of the outer membrane (most
specifically the lipopolysaccharide, LPS, in gram negative bacteria) and the natural activity of efflux pumps.
Multidrug-efflux pumps are also a common mechanism of induced resistance [21],[22]. Table 2 shows some
examples of bacteria with intrinsic antimicrobial resistance.
Mechanisms of resistance

• Antimicrobial resistance mechanisms fall into four main categories: (1) limiting
uptake of a drug; (2) modifying a drug target; (3) inactivating a drug; (4) active
drug efflux. Intrinsic resistance may make use of limiting uptake, drug
inactivation, and drug efflux; acquired resistance mechanisms used may be drug
target modification, drug inactivation, and drug efflux. Because of differences in
structure, etc., there is variation in the types of mechanisms used by gram
negative bacteria versus gram positive bacteria. Gram negative bacteria make use
of all four main mechanisms, whereas gram positive bacteria less commonly use
limiting the uptake of a drug (don't have an LPS outer membrane), and don't have
the capacity for certain types of drug efflux mechanisms (refer to the drug efflux
pumps later in this manuscript) [26],[27]. Figure 2 illustrates the general
antimicrobial resistance mechanisms.
SIDE EFFECTS
• Antibiotics are screened for any negative effects before their approval for clinical use, and are usually
considered safe and well tolerated. However, some antibiotics have been associated with a wide extent of
adverse side effects ranging from mild to very severe depending on the type of antibiotic used, the microbes
targeted, and the individual patient.[38][39] Side effects may reflect the pharmacological or toxicological
properties of the antibiotic or may involve hypersensitivity or allergic reactions.[4] Adverse effects range from
fever and nausea to major allergic reactions, including photodermatitis and anaphylaxis.[40]
• Common side-effects of oral antibiotics include diarrhea, resulting from disruption of the species
composition in the intestinal flora, resulting, for example, in overgrowth of pathogenic bacteria, such as
Clostridium difficile.[41] Taking probiotics during the course of antibiotic treatment can help prevent
antibiotic-associated diarrhea.[42] Antibacterials can also affect the vaginal flora, and may lead to overgrowth
of yeast species of the genus Candida in the vulvo-vaginal area.[43] Additional side effects can result from
interaction with other drugs, such as the possibility of tendon damage from the administration of a
quinolone antibiotic with a systemic corticosteroid.[44]
• Some antibiotics may also damage the mitochondrion, a bacteria-derived organelle found in eukaryotic,
including human, cells.[citation needed] Mitochondrial damage cause oxidative stress in cells and has been
suggested as a mechanism for side effects from fluoroquinolones.[45] They are also known to affect
chloroplasts.[46]
Is the routine practice of antibiotic prescription and
microbial culture and antibiotic sensitivity testing
justified in primary maxillofacial space infection
patients? A prospective, randomized clinical study
• Abstract
• Purpose
• The purpose of this prospective, randomized, comparative clinical study was to compare treatment outcome of removal of foci and incision and drainage, with
or without oral antibiotic therapy, in the management of single primary maxillofacial space infection with a known focus.
• Materials and methods
• A total of 40 patients with single primary maxillofacial space infection with a known infectious focus were divided into two groups, one treated with
incision and drainage only, and the other with incision and drainage along with oral antibiotics. The focus of infection was addressed in both groups.
Parameters evaluated included pain score, maximum mouth opening, swelling, purulent discharge and return to normal life, which were assessed on days 1, 2,
3, 5 and 7. The patients were followed up until they reported return to normal life as assessed by a questionnaire.
• Results
• All of the patients rapidly responded to treatment as observed by a reduction in pain, swelling, discharge, and improvement in mouth opening. Pus discharge
stopped within first 3 days in 75% of patients. The patients who underwent immediate extraction showed a faster resolution of infection (mean return to
normal life = 9 days) than others (mean = 11.2 days). There was no statistically significant difference between the two groups for the five study parameters
(p < 0.05). Of the total pus specimens, 75% had no significant bacterial growth, or grew ‘oral flora’/contaminants, while only 25% grew specific bacteria.
• Conclusion
• This study questions the conventional practice by dental practitioners and surgeons of prescribing antibiotics to all patients with odontogenic infection.
Microbial culture and antibiotic sensitivity is of little therapeutic value in selected patient groups.
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