This section will outline some of the principles of antibiotic therapy and discuss the commonly used agents in ENT practice. The suggested treatment regimes are not exhaustive and prescribing antibiotics should always take into consideration the local sensitivity profiles for the infecting organisms.

The choice of an antibacterial compound for a particular patient and a specific infection is based on several factors: the pharmacokinetic profile of the antibiotic, the adverse effect profile, the site of infection, the sensitivity profile of the infecting organism, the patient’s immune status, evidence of efficacy from well conducted trials, the cost of the regime, and the patient’s history of allergy to antibiotics. The local sensitivity profile, where available, is useful when empiric treatment is being considered.

Minimum inhibitory concentration (MIC) is the lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism after overnight incubation. An adequate antibiotic dose should aim to achieve a concentration of antibiotic in the infected tissue that exceeds the MIC by three to four times for at least 75% of the time between successive doses. However, when the infection is located in a site where penetration is poor, such as an abscess cavity in the neck or in complicated sinusitis, drainage of pus collection is paramount. Sometimes, despite adequate MIC at the site of infection, activity may be reduced due to the local environment, such as an unfavourable pH.

Antibiotics inhibit or abolish the growth of microorganisms (bacteria and fungi) through a number of mechanisms, as shown in Table 3.1. Antibacterials are broadly classified into bactericidals, that kill bacteria directly, and bacteriostatics, which prevent them from dividing. However, these classifications are based on laboratory behaviour and, in practice, both classes are capable of ending a bacterial infection. In the treatment of most ENT infections acquired in the community, the choice of either a bacteriostatic or bactericidal antibiotic is of limited importance. However, in patients with severe infection, especially in immunocompromised states, a bactericidal agent must be used.

Acquired resistance commonly occurs through one of the following mechanisms: production of drug-inactivating enzymes (e.g. β-lactamase production by Haemophilus influenzae), alteration of the target site (e.g. penicillin binding protein in methicillin-resistant Staphylococcus aureus [MRSA]; 2.27, 2.28), and mechanisms which prevent access of the drug to the target site (e.g drug efflux pumps and poor cell wall permeability seen in Pseudomonas aeruginosa). Resistance can be passed on horizontally (e.g. by plasmid transfer) or vertically (by mutation). Knowledge of resistance patterns in the local environment is important and multi-disciplinary working with microbiologists is important in planning the treatment regime for serious infections. Clinical vigilance is necessary to reduce the emergence of resistant strains (Table 3.2).

While parenteral administration improves the bioavailability of a drug, it is associated with an increased risk of adverse effects. Thus, parenteral administration should be reserved for patients who are severely ill (e.g. acute mastoiditis) or in situations where oral intake is not possible (e.g. quinsy). Oral treatment can be commenced once the patient shows clinical improvement.