Chapter 27 Bacterial Infections (2024)

KEY TERMS AND DEFINITIONS

LEARNING OBJECTIVES

After completing this chapter, you should be able to

1. Define:

   • Infection

   • Bacteria

   • Normal flora

   • Pathogen

   • Resistance

2. Outline the concept of normal flora bacteria and the mechanism behind the development of pathogenicity.

3. Describe host defense mechanisms.

4. Recognize the types of bacteria and bacterial infections.

5. Explain the therapeutic effects of antibiotics and the most common indications for each class.

6. Identify factors relevant to antibiotic selection.

7. Outline the management of patients with bacterial infections, including monitoring for efficacy and safety.

Bacteria are single-celled microscopic organisms that live in soil, water, and humans. Bacteria are found everywhere on earth and in all types of environments. There are approximately five nonillion (5 × 10³⁰) bacteria on earth.1

In humans, bacteria reside on the skin and in the digestive tract, genitourinary tract, airways, and mouth. When these bacteria stay in a particular part of the body and do not cause harm or infection, they are referred to as normal flora or colonizing bacteria. Normal flora protects the body against disease-causing organisms. Normal flora also performs tasks that are useful to the human host. Skin flora prevents pathogenic organisms from colonizing the surface of the skin by utilizing nutrients for themselves and/or being hostile to pathogenic organisms. The flora that resides in the gastrointestinal (GI) tract are often referred to as gut flora. These organisms are responsible for many functions, such as preventing the overgrowth of pathogenic organisms, carbohydrate metabolism, production of certain vitamins (biotin, vitamin K), and various other functions. It is important to understand that not all bacteria are infectious when they reside in their normal environment and that they perform many important functions.

Bacteria that cause illness or disease are known as pathogens; they are referred to as pathogenic. Bacteria become pathogenic when they produce toxins and/or gain access to a body location where they are not tolerated as normal flora. Toxin production or invasion by pathogenic organisms are considered infection. Many host factors may influence the likelihood of infection. Host defense mechanisms can be classified as natural barriers, nonspecific immune responses, and specific immune responses.

Natural barriers to infection include the skin, mucous membranes, respiratory tract, and GI tract. The skin usually provides protection unless its barrier is physically disrupted (eg, injury, abrasion, incision, burns, or intravenous catheter). Mucous membrane barriers include secretions that are produced by the body (eg, cervical mucus, tears, or saliva). Many of these secretions contain immunoglobulins, which are proteins that are used by the immune system to identify and neutralize foreign substances, such as IgA and IgG that prevent organisms from attaching to host cells. The respiratory tract barrier consists of cilia (short hair-like structures that extend from a cell and move in locomotion). The lining of the respiratory tract serves as a filter mechanism as it transports invading organisms away from the lung. In addition, coughing serves as a barrier to remove these organisms. GI barriers include the acidic content of the GI tract and antibacterial activity of pancreatic enzymes, bile, and secretions released by the intestine. As mentioned earlier, the normal flora of the GI tract can serve as a barrier because they inhibit pathogenic organisms by competing for environmental resources.

Once a pathogenic organism is recognized, the body’s natural defenses are initiated. Nonspecific immune responses are usually produced first. This response involves fever and the increased production of neutrophils, WBCs capable of ingesting microorganisms or particles (discussed in Chapter 25). The inflammation that occurs during an infection directs the immune system response to the site of injury or infection by increasing blood flow to that site and increasing vascular permeability. This allows the WBCs to penetrate tissues and access the site to begin inhibiting the spread of the infectious organism.

Specific immune responses occur after infection. The body produces antibodies and immunoglobulins that adhere to specific targets on the infecting organisms. The antibodies help cells ingest antigens, inactivate toxic substances that are produced by bacteria, and attack bacteria directly. In addition, the specific immune response activates systems responsible for clearing pathogens from a host.

When there are breakdowns or deficiencies in the body’s defense system, the host is vulnerable to many types of infections. Defects in natural barriers include impaired cough, loss of gastric acidity, loss of cutaneous (skin tissue) integrity, and loss of normal flora. Defects in immune barriers, which include disease states that limit or inhibit the production or replication of the body’s immune cells, are referred to as immunosuppression or immunodeficiency. Diseases, such as HIV infection, lupus, leukemia, and megaloblastic anemia, and decreases in numbers of WBCs lead to immunosuppression. Additionally, certain medications can contribute to deficiencies in the host’s immune response. These medication classes include some cancer chemotherapies, some biologics, and corticosteroids.

Signs and Symptoms of Bacterial Infections

Signs and symptoms in the infected host are based on the location and the type of infection. Infection can be confirmed by fever, other signs and symptoms, and predisposing factors. Fever is defined as a controlled elevation of body temperature above the normal range of 36°C to 37.8°C (98.2°F to 99.5°F). The increase in body temperature is a defense mechanism. Some organisms are susceptible to moderate temperature elevations and, in addition, the elevation of temperature activates many of the body’s other defense mechanisms. Recall from Chapter 25 that certain WBCs are responsible for providing defense against invading pathogens. Most infections cause an elevation of the body’s WBC count, known as leukocytosis.

Identification of the pathogen assists with confirming the presence of infection. Infected body materials are often sampled for this purpose. Such sampling is known as culturing. It is most effective if cultures are obtained prior to antibiotic therapy.

Several types of cultures can be obtained from the infected host. These include blood, sputum, tissue, wound, urine, stool, cerebral spinal fluid, and samples from other body fluids. The interpretation of the culture is important in determining whether the organisms identified (if any) are pathogenic, contaminant, or normal flora from the site of collection. Another test used to assist in obtaining useful information regarding the type of organism present is known as a Gram stain. Gram staining rapidly classifies bacteria into broad groups based on their shape and color and may provide useful information to assist in the initial selection of antibiotic therapy before culture results are completed.

For certain types of infections, such as pneumonia, other methods can be used to diagnose or confirm the presence of infection. This includes chest x-rays to review the patient’s lungs for images that may reveal infiltration in the lobes of the lung. Computed tomography (CT) scans along with magnetic resonance imaging (MRI) can allow the clinician a better view of infectious processes in many parts of the body.

There are many different types of infections that occur in humans. Bacterial infections can form in every system of the human body. Table 27-1 classifies various types of infections, location, and some of the most common signs and symptoms.

Classification of Bacteria

There are several types of bacteria that are responsible for causing infections. The classification of bacteria includes the association of bacteria into an organized form of naming referred to as taxonomy. This includes the genus and species names of the bacteria. For example, with the bacterium known as Staphylococcus aureus, Staphylococcus is the genus or family name and aureus is the specific species. In addition, bacteria are classified by their shapes, known as morphology. There are three basic morphologies of bacteria: round (coccus), rod-shaped (bacillus), or spiral-shaped (spirillum). Bacteria are also classified by their color after a stain is applied. This staining process is referred to as a Gram stain. As mentioned previously, Gram staining is an empirical method of differentiating between the main groups of bacteria: Gram positive, Gram negative, and acid fast. Gram-positive bacteria have a thick cell wall that stains purple. Gram-negative bacteria have a thin cell wall that stains pink. Acid-fast bacteria resist Gram staining because the cell walls contain a high concentration of lipids. Finally, bacteria can be classified based on oxygen requirements. Those bacteria that require oxygen to live and grow are referred to as aerobic and those not needing oxygen are referred to as anaerobic.

The two most common groups of Gram-positive cocci (round) are staphylococci and streptococci. These are the genus names and there are several species within each group. When viewed microscopically, staphylococci appear in clumps (clusters) like a bunch of grapes and streptococci form chains. The most common pathogen in the Staphylococcus group is Staphylococcus aureus. Further tests can differentiate Staphylococcus aureus from other staphylococci. All species of staphylococci are normal flora and colonize on the skin and mucous membranes of humans.

Streptococci are classified according to their ability to break down blood in fresh blood agar plates. Some streptococci have no effect on blood and are termed nonhemolytic streptococci. The most important of the nonhemolytic streptococci are the enterococci, such as Enterococcus faecalis and Enterococcus faecium, both of which are normal flora in the GI tract. Other streptococci cause partial breakdown of blood and are called alpha-hemolytic streptococci, which are often referred to as viridans (green) streptococci. The viridans streptococci are a large and heterogeneous group of bacteria and include organisms that play a role in tooth decay and those that can cause endocarditis (infection of the tissue surrounding the heart) and brain abscesses. The most common pathogen of the alpha-hemolytic streptococci family is Streptococcus pneumoniae (the cause of pneumococcal pneumonia and meningitis). The beta-hemolytic streptococci cause the complete breakdown of blood in fresh blood agar plates. Clinically, the most important of the beta-hemolytic streptococci is Streptococcus pyogenes, the infecting organism for strep throat.

The Gram-positive bacilli (rods) can be divided according to their ability to produce spores. Spores of Gram-positive rods are highly resistant structures that may add considerably to their pathogenic capacity. Gram-positive rods that are spore forming are grouped in the genus Bacillus. Important members of this genus include Bacillus anthracis (the cause of anthrax) and Bacillus cereus (a cause of food poisoning). Gram-positive rods that are anaerobic spore formers are grouped in the class clostridia. These include Clostridium perfringens, a principal cause of gangrene, Clostridium tetani (the cause of tetanus), Clostridium botulinum (the cause of the fatal food poisoning botulism), and Clostridioides difficile (C. diff), a growing cause of infectious diarrhea following antibiotic therapy.

The non-spore-forming Gram-positive rods include coryneform bacteria and lactobacilli. Some lactobacilli are important members of the normal vagin*l flora of women of child-bearing age. A common pathogen of this group includes Listeria monocytogenes, which is one of the most virulent foodborne pathogens. Table 27-2 organizes the Gram-positive bacteria by shape, oxygen use (ie, aerobic or anaerobic), and enzyme-producing groups.

The Gram-negative bacteria have an outer thin cell wall and stain pink on a Gram stain. The Gram-negative cocci include the genera Moraxella and Neisseria.2 The most pathogenic Neisseria organisms include Neisseria meningitidis (the cause of bacterial meningitis) and Neisseria gonorrhoeae (the cause of gonorrhea). These organisms are most often seen in pairs and are commonly referred to as diplococci.

Gram-negative bacilli include the order enterobacterales. This group is differentiated into types based on whether they can grow in the presence (aerobic) or absence (anaerobic) of oxygen and are frequently found in the GI tract of humans and animals. Some pathogens in this group include Yersinia pestis (the cause of plague), Salmonella typhi (the cause of typhoid), Shigella dysenteriae (the cause of bacillary dysentery), Pseudomonas aeruginosa (the cause of many types of infections associated with high mortality rates), and Salmonella enteritidis (the cause of food poisoning). Additional members of this class include Escherichia coli and members of the genus Klebsiella. The Vibrio and Campylobacters are Gram-negative rods that appear curved or spiral in shape. These bacteria are commonly found in natural waters, both freshwater and marine. Vibrio cholerae (the cause of the waterborne infection cholera), Campylobacters (the cause of bacterial enteritis), and Helicobacter pylori (the cause of stomach ulcers) are common pathogens in this group.

Some Gram-negative bacilli appear so short that they often resemble cocci under the microscope. These are sometimes referred to as cocco-bacilli. This group includes members of the genera Haemophilus and Acinetobacter, the latter being a cause of hospital-acquired (nosocomial) infections. Other Gram-negative bacteria are very fastidious (specific) in their nutritional requirements, including members of the genus Legionella, which cause atypical pneumonias and Legionnaires’ disease. Anaerobic Gram-negative bacilli include the genus Bacteroides, which causes infections of the peritoneal (abdominal) cavity and GI tract, and Fusobacteria, which causes periodontal (gum) infections. Table 27-3 organizes the Gram-negative bacteria by shape, oxygen use, and enzyme-producing groups.

The next group of bacteria includes the acid-fast bacteria, which possess a waxy cell wall, and they rarely stain using the basic Gram stain technique. These bacteria are identified using a different technique of staining that requires acid and alcohol. The most pathogenic organisms in this group include Mycobacterium tuberculosis, which causes tuberculosis, and Mycobacterium leprae, which causes leprosy.

A final group of bacteria is referred to as atypical. They are smaller in size than normal bacteria. The most common pathogenic forms are those in the Mycoplasma, Chlamydia, and Rickettsia groups. Mycoplasma lack cell walls and are highly pleomorphic, meaning they can change shape. The most common pathogen is Mycoplasma pneumoniae, which can cause both upper and lower respiratory infections, including tracheobronchitis and atypical pneumonia. Members of the genus Chlamydia have cell walls and are coccoid in shape. The most common pathogen in this group is Chlamydia trachomatis, a cause of female reproductive problems, pelvic inflammatory disease (PID), and neonatal respiratory and eye infections. The rickettsiae appear as pleomorphic (form-changing) bacillary or coccobacillary (short rod or oval) forms. The most common pathogens in this group include Rickettsia rickettsii, the cause of Rocky Mountain spotted fever (transmitted by ticks), and Rickettsia prowazekii, the cause of epidemic typhus fever (transmitted by infected human body lice).

Bacterial Resistance

When antibiotics first came into use in the 1930s, they were effective against most bacterial infections. Over time, many antibiotics have lost effectiveness against common bacterial infections due to the increase of antibiotic resistance. Bacteria may be naturally resistant to different classes of antibiotics or may acquire resistance from other bacteria through the exchange of resistant genes. Bacteria can be resistant to antibiotics in many ways. There are four main mechanisms by which bacteria exhibit resistance to antibiotics:

1. Inactivation or modification of the antibiotic—Bacteria produce enzymes that deactivate the antibiotic (eg, bacteria produce an enzyme called beta-lactamase that inactivates penicillins).

2. Alteration of the target site for the antibiotic—For example, penicillin binds to penicillin-binding protein (PBP) on some bacteria, but certain bacteria have altered this protein and the antibiotic cannot bind to the organism.

3. Alteration of metabolic pathways—For example, sulfonamide antibiotics work by disrupting the synthesis of folic acid by altering para-aminobenzoic acid (PABA). Some sulfonamide-resistant bacteria are able to utilize preformed folic acid and are not dependent on PABA for folic acid synthesis.

4. Reduction of drug transport across the cell wall—This occurs by genetic alterations in certain bacteria that decrease the permeability of the cell wall to the drug or increases active efflux (pumping out) of the antibiotic across the surface of the cell.

Susceptibility

Susceptibility refers to the sensitivity of a microorganism to a given antibiotic. Susceptibility testing is often used to determine the likelihood that a particular antibiotic regimen will be effective in eliminating or inhibiting the infection. Susceptibility testing is performed by growing the bacterial isolate in the presence of varying concentrations of several antimicrobials and then examining the amount of growth to determine which concentrations of antimicrobials inhibit the growth of the bacteria. Results are reported as susceptible (likely to inhibit the pathogenic microorganism), intermediate (may be effective at a higher-than-normal concentration), and resistant (not effective at inhibiting the growth of the organism). The organism is categorized as susceptible, intermediate, or resistant by determining the minimum inhibitory concentration (MIC) of the antibiotic. The MIC is the lowest concentration of an antibiotic that inhibits the growth of the bacteria. This information is then used to determine the best option for treating the infection. While broad-spectrum antibiotics are often ordered as initial therapy (to begin treatment of an apparent infection before all tests are complete), prolonged or inappropriate use of such agents can lead to antibiotic resistance, and more specific therapy is generally prescribed once the susceptibility of the infecting organisms has been determined.

Antibiotic Medications

Antibiotics are the drugs of choice for the treatment of bacterial infections. The goal of antibiotic therapy is to kill invading bacteria without harming the host. Antibiotic effectiveness depends on the mechanism of action of the antibiotic, distribution of the drug to the site of infection, immune status of the host, and resistance patterns of the organism.

The first class of antibiotics discussed here are those that are categorized in the beta-lactam group (because they have a beta-lactam ring in their chemical structure). Beta-lactam antibiotics work by inhibiting cell wall synthesis of bacteria. The first antibiotic class in this group to be discovered was penicillin. It was discovered by Alexander Fleming in 1928 and developed as a treatment for human infections in the late 1930s.3 Over the years, as a result of research prompted by bacterial resistance, the beta-lactam class has grown into several groups with various spectra of activity (ie, activity against specific types of microorganisms).

Penicillins are bactericidal. They kill bacteria by activating enzymes that destroy the bacterial cell wall.3 Some organisms produce beta-lactamase, an enzyme that inactivates penicillins. This effect can be blocked by adding a beta-lactamase inhibitor (clavulanic acid, sulbactam, or tazobactam) to the penicillin. Penicillins are primarily used for Gram-positive organisms and some Gram-negative cocci. A minority of Gram-negative bacilli are also susceptible to large parenteral (intravenous, or IV) doses of penicillin.

All classes of penicillins have the same adverse effects and reaction, which include anaphylaxis, drug-fever, serum sickness, rash, nephritis, hemolytic anemia, and leucopenia. Side effects patients may experience when taking these medications include diarrhea, colitis, nausea, and vomiting. Most of the penicillins are renally excreted and dose modifications are necessary for patients with impaired kidney function. The lists that follow detail the characteristics of the major groups of penicillin antibiotics. Pronunciations, brand names, and dosage forms for these agents are detailed in Medication Table 27-1 (Medication Tables are located at the end of the chapter).

Antibiotic Selection

Several factors must be considered for antibiotic selection. First, the clinician must determine the goal of therapy. In some cases, this will be to prevent an infection following surgery or another procedure. This is known as surgical prophylaxis. Not all surgeries or procedures require the patient to receive antibiotic therapy. Treatment with antibiotics is recommended for patients with valvular heart disorders or artificial joints, as well as those who are immunosuppressed, or otherwise at high risk for infection. Procedures carrying a higher risk of bacterial infections are those performed in the mouth, GI tract, and genitourinary tract. If prophylactic antibiotic therapy is indicated, antibiotic selection is based on the normal flora that resides in the location of the procedure. For example, a patient at risk for endocarditis (infection of the heart valves or lining of the heart) who is scheduled for a dental procedure would receive amoxicillin 2,000 mg orally 30–60 minutes prior to the procedure. Amoxicillin has activity against those organisms that inhabit the oral cavity. The goal of using amoxicillin in this patient is to prevent the bacteria that enter the bloodstream (from the dental procedure) from causing an infection in the heart. As stated earlier, not all patients need antibiotic prophylaxis; it is routinely used for those with risk factors for infectious processes. There are several guidelines available for prophylactic antibiotic dosing for various procedures.

In other cases, the goal of therapy will be to treat an infection that has already developed. Regardless of the goal, antibiotic selection is determined by the most likely organism to cause an infection based on the location of the infectious process or type of surgery performed. Empiric therapy refers to the selection of an antibiotic based on the organisms most commonly encountered at the site of the infection prior to obtaining culture results. Finally, definitive treatment refers to antibiotic selection that has activity toward a known pathogen based on the results of culture and sensitivity testing. In addition, the following factors must be considered for antibiotic selection.

• Allergies or history of adverse drug reactions to certain antibiotics (cross-sensitivity of antibiotic class)

• Patient’s age (FDA approval for specified ages or known toxicity within certain age groups)

• Genetic or metabolic abnormalities (drug accumulation/toxicity)

• Renal (kidney) function (dose adjustment if renally excreted)

• Hepatic (liver) function (dose adjustment if hepatically metabolized)

• Site of infection (drug distribution/tissue penetration)

• Pregnancy/lactation (safe use in pregnancy or lactation)

• Concomitant drug therapy (drug interactions)

• Concomitant disease states (drug/disease interaction)

• Antibiogram (hospital-specific susceptibility and resistance patterns)

• Resistance patterns

Combination Therapy

Combination therapy refers to the use of more than one antibiotic to treat an infection. The concept behind combination therapy is to achieve one of the following: broaden antimicrobial coverage for a suspected organism or multiple organisms, improve efficacy though synergistic activity, and help overcome bacterial resistance. Many infections, such as pneumonia and hospital-acquired (nosocomial) infections, are treated with combination therapy for the reasons listed earlier. In addition, when patients are started on empiric therapy and the organism is yet to be identified, they may be placed on multiple antibiotics until the cultures and sensitivities are reported. At that time, the clinician may narrow down the antibiotic regimen based on the results and patient response.

Patient Monitoring

Patient monitoring begins once antibiotic therapy is initiated. This includes monitoring the patient for safety, efficacy, response, and completion of therapy. Safety monitoring includes watching for both allergic reactions and adverse drug events associated with the selected antibiotic(s). As with all medications, the patient’s allergies must be reviewed prior to any medication being dispensed. Antibiotic allergies range from nausea to anaphylaxis. If a patient is allergic to penicillin, there is a small chance of cross allergy to other antibiotics in the beta-lactam class. For mild reactions to penicillins, such as nausea or a mild rash, most clinicians will confidently dispense an antibiotic in a different beta-lactam group, such as a cephalosporin. If the patient reports an incident of anaphylactic reaction to penicillin, an antibiotic from a different class altogether (ie, fluoroquinolone) should be used to ensure patient safety. Allergies are often a class effect and antibiotics from a different class should be used for severe allergies to avoid additional reactions.

In addition to allergies, patients should be monitored for adverse drug reactions. It is important for clinicians to be familiar with the common side effects of different antibiotic classes to be able to properly monitor the patient. Adverse reactions to antibiotics include the side effects one may experience while taking the medication. They can also be the result of a drug interaction that increases the chance of a known adverse reaction or unwanted effect due to altered drug absorption, distribution, and elimination.

It is important for clinicians to monitor patients for response to antibiotic therapy, ensuring efficacy of the antibiotic(s) selected to treat the infection. As mentioned earlier, cultures are obtained to help identify the pathogenic organism(s). These cultures are monitored for growth, identification, and sensitivity of the organism to specific antibiotics. Commonly, cultures may remain negative and no organism(s) grow in the culture obtained. If this is the case, the patient’s laboratory and physical condition will be monitored to determine the efficacy of the selected therapy. In cases where cultures do grow, the clinician will review the identified organism(s) and compare it to the antibiotic regimen the patient is receiving to ensure proper antimicrobial coverage. If sensitivities are reported, the clinician may modify the regimen to an antibiotic that is more effective against the specific pathogen. Whenever possible, therapy is adjusted to provide coverage for only those organisms isolated or suspected. This is an important factor in reducing the possible development of resistant organisms.

Patient-specific values, such as the WBC count and temperature, are monitored closely to determine if the patient is responding to antibiotic therapy. A baseline WBC count is obtained and monitored closely thereafter. If the WBC count trends downward, it is a good indication the patient is responding to antibiotic therapy and improving. If the patient’s WBC count increases or continues to increase despite antibiotic therapy, it may be a sign of treatment failure. A patient’s temperature is also monitored for response to therapy. Like the WBC count, if the temperature was elevated at baseline and the patient becomes afebrile and maintains an afebrile state, it is a good indication that the patient is responding to therapy. Alternatively, if the temperature remains elevated or spikes, it may be a sign of treatment failure.

Finally, other diagnostic tests may be reordered to evaluate for continued or worsening infection. A repeat chest x-ray can be obtained for patients who are worsening on therapy to determine if the initial infection has not responded or if there may be a new infection that may warrant a change in therapy. Clinicians must also determine duration of therapy for antibiotic use based on the type and severity of infection being treated. There are several guidelines available for various infections that serve as treatment suggestions for both selection of antibiotic therapy and duration of treatment. Although these guidelines provide recommendations for duration of therapy, it is important to also evaluate the clinical response of the patient and adjust the duration based on response. In some cases, a longer duration of therapy may be warranted.

Duration of treatment is not only important to prevent treatment failure but also to help prevent antibiotic resistance. Often patients start to feel better and do not finish their course of antibiotics. This may lead to bacterial resistance as the pathogenic organism(s) may not be completely eradicated.

Prevention of infection is the best and most effective medicine. Handwashing is the most important and effective way to limit the spread of infectious organism(s). In hospital settings, many measures are in place to limit the number of hospital-acquired infections. These include the proper use of hand sanitizer, surveillance of employee handwashing, limiting contact with patients with highly contagious organisms (known as isolation), and monitoring of patients’ IV and urinary catheters, which can increase the risk of patients getting a hospital-acquired infection.

SUMMARY

Bacteria live among us and reside in our bodies as normal flora that helps us fight off other invading organisms and assist with many important functions in various organ systems. Our bodies have various natural defenses that assist normal flora in providing protection against invading organisms. When these natural defenses fail or breakdown, normal flora can become pathogenic and cause infection. Once an infection occurs, the body’s immune system starts the process of attacking the pathogen and inhibiting the replication of the pathogen. Every system in the body is susceptible to infection. In most cases, patients are febrile and have elevated WBCs that are consistent with infection. The location of the infection determines the type of disease or illness that occurs. The patient usually exhibits signs and symptoms that are specific to the type of infection. The signs and symptoms of the infection can guide the clinician regarding the most likely organism causing the infection. Depending on the type of infection and patient history, empiric antibiotic therapy is initiated. If bacterial resistance is suspected, broader coverage may be initiated. Risk factors for bacterial resistance include recent prior antibiotic use, and history of prior resistant organisms. Samples from the patient are usually cultured in hopes of identifying the offending organism and also to determine the susceptibility of that organism to various antibiotics. When the cultures reveal the infecting organism(s), the initial empiric therapy can be changed, if necessary, to agents chosen to treat the specific infection.

There are several antibiotic classes that cover specific organisms and each has specific indications for use. Once antibiotic therapy is initiated, patients are monitored for safety and for efficacy. Safety includes monitoring for allergic reactions and adverse reactions or side effects. Efficacy refers to signs of improvement and eradication of the organism(s). Monitoring cultures and sensitivities allows the clinician to modify empiric therapy to target the specific organism(s) identified and use the most effective agent based on sensitivities. A patient’s vital signs and laboratory values allow the clinician to determine if a patient is improving.

Over the years, bacteria have “learned” many methods to become resistant to antibiotics. Every year new antibiotics are developed to combat resistant organisms but not at the rate of bacterial resistance that is occurring. One way to slow the development of resistance is with the proper use of antibiotic regimens, with clinicians choosing an agent with the narrowest spectrum that includes the infecting organism and treating the infection for the optimal length of time.

REVIEW QUESTIONS

1. What are some ways that bacteria become resistant to antibiotics?

2. What factors should be considered when selecting an antibiotic to treat an infection?

3. Describe the difference between using antibiotics for surgical prophylaxis and empiric treatment of an infection.

4. Why is it important for patients to finish their full prescribed course of antibiotics even if it extends for several days after they feel completely better?

5. Why are beta-lactamase inhibitors added to penicillins but not to fluoroquinolones?

MEDICATION TABLES