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For any reason, everyone is taking antibiotics without a doctor’s prescription. We will explain to you when to take antibiotics.

Before I tell when to take antibiotics, you should have an idea about various antibiotics.

History of Antibiotics

The first researchers to understand the clinical potential of microorganisms as remedial agents were Pasteur and Joubert, who recorded their searches way back in 1877.

The current era of the chemotherapy of infection began with the clinical use of Prontosil, a sulfonamide dye by Domagk in 1935. Sir Alexander Fleming’s serendipity of penicillin in 1929 at St. Mary’s Hospital in London is considered as one of the most well-known discoveries of that century. Chain and Florey then redeemed it (penicillin), and clinical use in 1941 started the Golden age of antimicrobial therapy. In the 1940’s Waksman and his colleagues created streptomycin from a group of soil microbes.All three clubs of scientists – Domagk; Fleming-Chain-Florey; Waksman got Nobel prize for their discoveries.

Definition

Antibiotics are synthetic things created by various classes of microorganisms that suppress the growth of or destroy other microorganisms at very low concentrations. However, nowadays, synthetic antibacterial agents that are not outputs of microbes are also termed as antibiotics.

 Classification

There are various ways used to classify and arrange antimicrobial agents, and all are hampered by exceptions and extensions. Historically, the most popular classification has been based on chemical composition and proposed the mechanism of action:

1 Agents that repress the synthesis of or stimulate enzymes that interrupt bacterial cell walls to produce a loss of viability and frequently cell lysis. 

E.g.: Penicillins, cephalosporins, etc.

2 Agents that act instantly on the cell membrane of the microorganism, altering permeability and commencing to leakage of intracellular compounds.

E.g.: Detergents, antifungal agents like Nystatin, Amphotericin-B, etc. 

3 Agents that change the function of bacterial ribosomes to cause reversible interference of protein synthesis; i.e. bacteriostatic drugs 

E.g.: Chloramphenicol, erythromycin tetracyclines, etc.

4 Agents that bind to the 30 S ribosomal subunit and modify protein synthesis pointing to cell death 

E.g.: aminoglycosides.

5 Agents that affect nucleic acid metabolism 

E.g.: Rifamycins, metronidazole.

 6 The antimetabolites, i.e. agents that obstruct specific metabolic steps that are necessary to microorganisms. 

E.g. trimethoprim, sulfonamides.

7 Nucleic acid analogs – agents that connect to viral enzymes that are required for DNA synthesis thus preventing viral replication. 

E.g. : Zidovudine – Acyclone

II. Types of organisms against which primarily active

1. Antibacterial : Penicillins, etc.

2. Antifungal : Ketoconazole etc.

3. Antiviral : Acylovir etc.

4. Antiprotozoal : Metranidazole etc.

5. Antihelmintic : Mebendazole etc.

III. Based on spectrum of activitiy

1. Narrow spectrum – Penicillin, Streptomycin.

2. Broad spectrum – Ampicillin, Tetracyclines.

Know when to take antibiotics

Indications, when to take antibiotics, are : 

It is most important that an antibiotic is used to treat an infection.

1) If it looks likely that delaying the antibiotic will result in failure to efficiently operate severe or possibly life-threatening infection.

2) When the patient is immunocompromised or is at increased risk because of a systemic condition.

The use of antibiotics should be based on clinical evaluation and the judgment that antimicrobial therapy will have a beneficial/therapeutic effect. Therapy should help contain and limit the further expansion of the infection, decrease duration and discomfort, or reduce risks of systemic association or complications.

Antibiotics should clearly be held for patients with oro-facial infections when one or more of the following related signs, symptoms, or conditions are present.

1) Flush and or colds, current or in the last 24 hours.

2) Uneasiness, exhaustion, weakness, dizziness, rapid respirations, or other debilitation.

3) Trismus or Jaw pain.

4) Cellulitis, infection extending acutely (e.g. within 24 hours)characterized by fever, pain, and swelling into adjacent spaces or tissues without clearcut localization.

5) Local systemic infection with a history of rheumatic fever, endocarditis, heart prosthesis, or other predisposing factors.

6) Immuno-compromised status (e.g. AIDS, Cancer, etc.).

7) Allograph (cardiac, renal, bone marrow, liver and or osseous implants).

8) Diabetes mellitus or other contributory systemic diseases.

Situations in which antibiotics are not necessary

1) Uncomplicated edema induced by injury/chemicals.

2) Pain-related to tooth decay (pulpitis) or injury.

3) Well localized minor abscess that is likely to respond well to drainage and treatment of the local source of the infection, such as a periapical abscess.

4) Uncomplicated dry socket which happens after a traumatic tooth extraction.

5) Simple, well-defined pericoronitis during wisdom tooth pain.

6) Bacteria limited to a root canal.

7) Recurrent uncomplicated draining sinus tract linked with a non-vital tooth.

Which antibiotic to choose?

 The goal is to choose an antibiotic that is selectively active against the most likely infecting agents, and that has the least potential to cause allergic or toxic reactions in the specific patient under treatment.

 The choice depends on :

a. The patient

b. The infecting organism

c. The drug

A) Patient factors

1)    Age may affect the kinetics of many antibiotics. 

E.g., i) Tetracyclines are contraindicated below the age of 6 years (it discolor and weaken the teeth) 

ii)  Sulfonamides provoke kernicterus in neonates because their blood-brain barrier is more penetrable.

2)    Renal and hepatic role: Prudence use, and adjustment of the dose becomes important when the organ of its disposal is faulty.

I) Drugs to be avoided in renal failure – related to dentistry

1. Tetracyclines (except doxycycline)

Dose reduction needed

1. Aminoglycosides.

2. Metronidazole.

3. Cephalosporins.

II) In liver disease: Avoid Tetracyclines and Metronidazole

3)    Local factors :

1. Presence of pus and secretions.

2. Presence of necrotic material hematomas, foreign body.

3. Low pH at the site of infection.

 4)    Drug allergy: History of previous exposure to be taken.

5)    Impaired host defense.

6)    Pregnancy.

7)    Genetic factors: Chloramphenicol, sulfonamides are likely to produce hemolysis in G6PD deficient patients.

B) Organism related considerations

1) The clinical diagnosis itself directs the choice of the antibiotic.

2) The decision to be based on the bacteriological examination – by culture and sensitivity testing.

C) Drug factors

1) The spectrum of activity: Narrow/broad.

2) Type of activity: Bactericidal / bacteriostatic.

3) The sensitivity of the organism.

4) Toxicity.

5) Pharmacokinetics: for best action, the antibiotic has to be present at the location of the infection in sufficient intensity for an adequate span of time.

6) Route of administration: for less severe infections, an oral antibiotic is preferred, but for serious infections, a parenteral antibiotic may be chosen.

7) Evidence of clinical efficacy.

8) Cost.

 COMBINED USE OF ANTIBIOTICS

This is done only with a specific purpose, such as to achieve:

i) Synergistic action of the drugs.

ii) To reduce the severity/incidence of adverse effects.

iii) To prevent the emergence of resistance.

iv) To broaden the spectrum of antimicrobial action.

a) Treatment of mixed infection.

b) Initial treatment of severe diseases.

Disadvantages of combinations

i) Increased chances of superinfections.

ii) The emergence of resistance may be promoted.

iii) Increased chances of adverse effects.

iv) The increased cost of therapy.

Problems that arise with taking antibiotics:

1)    Toxicity:            a) Local irritancy – at the site of administration.

b) Systemic toxicity – dose-related and predictable 

E.g., Tetracyclines – Liver and kidney damage 

                                        Antianabolic effect

Aminoglycosides – 8th cranial nerve damage

                                     Kidney toxicity

Chloramphenicol – Bone marrow depression

2) Hypersensitivity reactions: Unpredictable and unrelated to dose – rashes to anaphylactic shock.

3) Drug resistance : 

1. Natural: E.g. gram-negative bacilli unaffected by penicillins.

2. Acquired.

It is the addition of endurance by an organism (which was sensitive before) due to the overuse of an antibiotic over a period of time.

This acquired resistance is by:

I] Mutation: It is a stable and heritable genetic change that occurs spontaneously and randomly among microorganisms. Any sensitive population of a microbe contains few mutant cells which need a high amount of the antibiotic for inhibition. These are selectively shielded and get a chance to propagate when the sensitive cells are killed by the antibiotic. Thus, in time, it would look that a sensitive strain has been replaced by a resistant one. It may be a

Single-step

Multi-step

II] Gene transfer: of 1 organism to different can happen by:

i) Conjugation: Transfer through sexual contact i.e. bridge formation, sex pilus.

ii) Transduction: through a bacteriophage (virus).

iii) Transformation: through DNA.

Mechanism of increased bacterial resistance to antibiotics:

i) Alteration of permeability of the bacterial cell for the drug.

ii) Changes in the target sites for the drug in the bacterial cell.

iii) Bypassing metabolic reactions blocked by the drug.

iv) Drug inactivation.

III] Cross-resistance : Inheritance of protection to one antibiotic conferring resistance to another antibiotic, to which the organism has not been exposed, is called cross-resistance. This is more commonly seen between chemically or mechanically related drugs.

Prevention of drug resistance

 No indiscriminate and inadequate or unduly prolonged use of antibiotics should be made.

 Proper rapidly acting and selective antibiotics whenever possible.

Combination antibiotics should be employed in situations of prolonged treatment.

 Infection by organisms wicked for evolving resistance must be managed intensively.

4)    Superinfection: Emergence of a new infection as a consequence of antimicrobial therapy.

The application of maximum antibiotics produces some change in the usual microbial flora of the body. The standard flora provides to host defense by developing substances called bacteriocins which hinder pathogenic organisms.

Moreover, frequently, the pathogen has to fight with the natural flora for nutrients, etc to build itself.

Absence of conflict may enable even a regularly non-pathogenic component of the flora, which is not frustrated by the drug to command and penetrate. More finish the destruction of body flora, higher are the risks of acquiring superinfection.

Hence, it is usually linked with the application of broad/extended-spectrum antibiotics such as tetracyclines, chloramphenicol, ampicillin, newer cephalosporins.

Superinfections are more prevalent when host defense is jeopardized, as in

– Corticosteroid therapy.

– Leukemias and other malignancies.

– AIDS

– Agranulocytosis.

– Diabetes, disseminated lupus erythematosus.

To minimize superinfections

a) Use specific antibiotics whenever possible.

b) Do not apply antimicrobials to manage self-limiting or viral infections.

c) Do not necessarily prolong antimicrobial therapy.

5)    Masking of an Infection: A short-term program of an antibiotic may be enough to manage one infection but only momentarily overcome another one contacted concurrently. The other infection will be cloaked initially, only to reveal later in a severe form.

The overuse of antibiotics can be dangerous. You should be a little proactive regarding when to take antibiotics.