Infection

INTRODUCTION

Despite improved treatments and prevention, including potent antibiotics, complex immunizations, and modern sanitation, infection still causes much serious illness, even in highly industrialized countries. In developing countries, infection is a critical health problem.

WHAT IS INFECTION?

Infection is the invasion and multiplication of microorganisms in or on body tissue that produce signs and symptoms as well as an immune response. Such reproduction injures the host by causing cellular damage from microorganismproduced toxins or intracellular multiplication or by competing with host metabolism. The host’s own immune response may increase tissue damage, which may be localized (as in infected pressure ulcers) or systemic. The infection’s severity depends on the pathogenicity and amount of the invading microorganisms and on the strength of the host’s defenses. The very young and the very old are most susceptible to infections.

Microorganisms that cause infectious diseases are difficult to overcome for many reasons:

Some bacteria develop a resistance to antibiotics.
Some microorganisms, such as human immunodeficiency virus, include many different strains and a single vaccine can’t provide protection against them all.
Most viruses resist antiviral drugs.
Some microorganisms localize in areas that make treatment difficult, such as the central nervous system and bone.

Also, certain factors that normally contribute to improved health, such as availability of good nutrition, clean living conditions, and advanced medical care, can actually lead to increased risk for infection. For example, travel can expose people to diseases that they have little natural immunity against. Increased use of immunosuppressants, surgery, and other invasive procedures also increases the risk for infection.

KINDS OF INFECTIONS

A laboratory-verified infection that causes no signs and symptoms is called a subclinical, silent, or asymptomatic infection. A multiplication of microbes that produces no signs, symptoms, or immune response is called a colonization. A person with a subclinical infection or colonization may be a carrier and transmit the infection to others. A latent infection occurs after a microorganism has been dormant in the host, sometimes for years. An exogenous infection results from environmental pathogens or sources other than the host; an endogenous infection results from the host’s normal flora (for instance, Escherichia coli displaced from the colon, which causes urinary tract infection).

PATHOPHYSIOLOGY How bacteria damage tissue

The human body is constantly colonized and often infected by bacteria and other infectious organisms. Some are beneficial, such as the intestinal bacteria that produce vitamins. Others are harmful, causing illnesses ranging from the common cold to life-threatening septic shock.

To infect a host, bacteria must first enter it. They do this either by adhering to the mucosal surface and directly invading the host cell, or by attaching to epithelial cells and producing toxins that eventually invade the host cells. To survive and multiply within a host, bacteria or their toxins adversely affect biochemical reactions in cells. This causes a disruption of normal cell function or cell death (see illustration below). For example, the diphtheria toxin damages heart muscle by inhibiting protein synthesis. Also, as some organisms multiply, they extend into deeper tissues and eventually gain access to the bloodstream.

Some toxins cause blood to clot in the smaller blood vessels. As a result, the tissues supplied by these vessels may become deprived of blood and subsequently damaged (see illustration below).

Other toxins can damage the cell walls of the smaller blood vessels, causing leakage. This fluid loss can result in decreased blood pressure, which in turn impairs the heart’s ability to pump enough blood to the vital organs (see illustration below).

Microorganisms responsible for infectious diseases include bacteria, viruses, rickettsiae, chlamydiae, fungi (yeasts and molds), and protozoa; larger organisms such as helminths (parasitic worms) may also cause infectious disease.

Bacteria are single-cell microorganisms with well-defined cell walls that can grow independently on artificial media without the need for other cells. Bacteria inhabit the intestines of humans and other animals as normal flora used in the digestion of food. Also found in soil, bacteria are vital to soil fertility. These microorganisms break down dead tissue, which allows it to then be used by other organisms.

Despite the many types of known bacteria, only a small percentage are harmful to man. (See How bacteria damage tissue.) In developing countries, where poor sanitation increases the risk of infection, bacterial diseases commonly cause death and disability. In industrialized countries, bacterial infections are the most common fatal infectious diseases.

Bacteria are classified by shape. Spherical bacterial cells are called cocci; rod-shaped bacteria, bacilli; and spiral-shaped bacteria, spirilla. Bacteria are also classified according to their response to staining (gram-positive, gram-negative, or acid-fast bacteria); their motility (motile or nonmotile bacteria); their tendency toward encapsulation (encapsulated or nonencapsulated bacteria); and their capacity to form spores (sporulating or nonsporulating bacteria).

Spirochetes are bacteria with flexible, slender, undulating spiral rods that have cell walls. Most are anaerobic. The three forms pathogenic in humans include Treponema, Leptospira, and Borrelia.

Viruses are subcellular organisms made up only of a ribonucleic acid or a deoxyribonucleic acid nucleus covered with proteins. They’re the smallest known organisms (so tiny they’re visible only through an electron microscope). Independent of host cells, viruses can’t replicate. Rather, they invade a host cell and stimulate it to participate in the formation of additional virus particles. The estimated 400 viruses that infect humans are classified according to their size, shape (spherical, rod shaped, or cubic), or means of transmission (respiratory, fecal, oral, or sexual).

Rickettsiae are relatively uncommon in the United States. They’re small, gram-negative organisms classified as bacteria that commonly induce life-threatening infections. Like viruses, they require a host cell (such as human or insect) for replication. Three genera of rickettsiae include Rickettsia, Coxiella, and Ehrlichia.

Chlamydiae are smaller than rickettsiae and bacteria but larger than viruses. They also depend on host cells for replication but, unlike viruses, they’re susceptible to antibiotics.

Fungi are single-cell organisms, with nuclei enveloped by nuclear membranes. They have rigid cell walls like plant cells but lack chlorophyll, the green matter necessary for photosynthesis; they also show relatively little cellular specialization. Fungi occur as yeasts (single-cell, oval-shaped organisms) or molds (organisms with hyphae, or branching filaments). Depending on the environment, some fungi may occur in both forms. Fungal diseases in humans are called mycoses.

Protozoa are the simplest single-cell organisms among animals. However, they show a high level of cellular specialization. Like other animal cells, they have cell membranes rather than cell walls, and their nuclei are surrounded by nuclear membranes.

In addition to these microorganisms, infectious diseases may also result from larger parasites, such as roundworms or flatworms.

MODES OF TRANSMISSION

Most infectious diseases are transmitted in one of four ways.

In contact transmission, the susceptible host comes into direct contact (as in contact with blood or body fluids) or indirect contact (contaminated inanimate objects or the close-range spread of respiratory droplets) with the source. The most common method of contact transmission is contaminated hands.
Airborne transmission results from the inhalation of contaminated aerosolized droplet nuclei (as in pulmonary tuberculosis).
In enteric (oral-fecal) transmission, the infecting organisms are found in feces and are ingested, in many cases through fecally contaminated food or water (as in salmonella infections).
Vector-borne transmission occurs when an intermediate carrier (vector), such as a flea, mosquito, or other animal, transfers an organism.

Many actions can be taken to prevent the transmission of infectious diseases, including:

comprehensive immunization (including required immunization of travelers to, or emigrants from, endemic areas)
drug prophylaxis
improved nutrition, living conditions, and sanitation
correction of environmental factors
widespread disease tracking

Immunization can now control many diseases, including diphtheria, tetanus, pertussis, measles, rubella, some forms of meningitis, poliovirus, hepatitis B, pneumococcal pneumonia, influenza, rabies, and tetanus. Smallpox (variola)—which killed and disfigured millions—was believed to have been successfully eradicated by a comprehensive World Health Organization program of surveillance and immunization. However, in light of recent concerns regarding bioterrorism, smallpox is considered a potential agent. Health care personnel must recognize potential cases of smallpox and initiate appropriate precautions as well as notify health department officials. Smallpox vaccination may be appropriate for certain emergency and firstresponse health care providers.

Vaccines, which contain live but attenuated (weakened) or killed microorganisms, and toxoids, which contain modified bacterial exotoxins, induce active immunity against bacterial and viral diseases by stimulating antibody formation. Natural active immunity is produced as a patient who has the disease forms antibodies against it, thus preventing the recurrence of the disease. Immune globulins contain previously formed antibodies from hyperimmunized donors or pooled plasma and provide temporary passive immunity. Generally, passive immunization is used when active immunization is perilous or impossible or when complete protection requires both active and passive immunization. It may also be appropriate in situations requiring immediate protection such as postexposure in which active immunity from immunizations takes too long to provide the necessary and immediate protection. Maternal passive immunity crosses the placental barrier from mother to fetus and is also provided to the infant by antibodies present in breast milk.

Standard precautions

The Centers for Disease Control and Prevention recommends that the following standard blood and body-fluid precautions be used for all patients. This is especially important in emergency care settings, where the risk of blood exposure is high and the patient’s infection status is usually unknown.

It’s important to remember that implementing standard precautions doesn’t eliminate the need for maintaining other transmission-based precautions designed for specific airborne, droplet, and contact infectious diseases.

Sources of potential exposure

Standard precautions apply to blood, semen, vaginal secretions, and cerebrospinal, synovial, pleural, peritoneal, pericardial, and amniotic fluids. Standard precautions also apply to other body substances, such as feces, urine, nasal secretions, saliva, sputum, tears, vomitus, and breast milk.

Barrier precautions

Wear gloves when touching blood and body fluids, mucous membranes, or the broken skin of patients; when handling items or touching surfaces soiled with blood or body fluids; and when performing venipuncture and other vascular access procedures.
Change gloves and wash hands after contact with each patient.
Wear a mask and protective eyewear, or a face shield, to protect the mucous membranes of the mouth, nose, and eyes during procedures that may generate the splatter of blood or other body fluids.
In addition to the mask and protective eyewear or face shield, wear a gown or an apron during procedures that are likely to cause splashing of blood or other body fluids.
After removing gloves and other protective equipment, thoroughly wash hands and other skin surfaces that may be contaminated with blood or other body fluids.

Precautions for invasive procedures

During all invasive procedures, wear gloves and a surgical mask and goggles or a face shield as appropriate.
During procedures that commonly cause droplets or splashes of blood or other body fluids, or for those that generate bone chips, wear protective eyewear and a surgical mask or a face shield.
During invasive procedures that are likely to cause splashing or a splattering of blood or other body fluids, wear a gown or an impervious apron.
If performing or assisting in a vaginal or cesarean delivery, wear gloves and a gown when handling the placenta or the infant and during umbilical cord care.
During spinal procedures (lumbar puncture, spinal and epidural anesthesia, myelogram), wear a face mask to prevent droplet spread of oral flora.

Work practice precautions

To prevent needle-stick injuries, don’t recap used needles, bend or break needles, remove needles from their disposable syringes or phlebotomy blood tube holders, or manipulate them.
Whenever possible use single-dose vials over multi-dose vials, especially when medications will be administered to multiple patients.
Use a sterile, single-use, disposable syringe and needle for each injection.
Use sharps safety devices. Activate safety mechanisms as directed.
Place disposable syringes and needles, scalpel blades, and other sharps items in punctureresistant containers for disposal. Make sure these containers are always located near the area of use.
Place large-bore reusable needles in a puncture-resistant container for transport to the reprocessing area immediately after a procedure.
If a glove tears or a needle-stick or other injury occurs, remove the gloves, wash your hands and the site of the needle-stick thoroughly, and put on new gloves as quickly as patient safety permits. Remove the needle or instrument involved in the incident from the sterile field. Promptly report injuries and mucous-membrane exposure to the appropriate infection control practitioner per facility protocol.

Hand hygiene, either by washing with soap and water or by sanitizing with an alcoholbased sanitizer, is recognized as the most effective method of interrupting the transmission of infection. Plain soap is adequate for removing visible soil. Antimicrobial soap is encouraged for washing after contamination with blood or body fluids. Alcohol-based hand sanitizers, which reduce the number of viable microorganisms on the hands, are designed for waterless use. In the United States, these products usually contain 60% to 95% ethanol or isopropanol.

Indications for washing with either ordinary or antimicrobial soap include:

when hands are visibly dirty or contaminated with proteinaceous material or visibly soiled with blood or other body fluids (even if gloves were worn)
before eating and after using the restroom
exposure to suspected or proven Bacillus anthracis (alcohol, chlorhexidine, iodophors, and other antiseptic agents have a poor potency against its spores)
after caring for a patient with Clostridium difficile (alcohol, chlorhexidine, iodophors, and other antiseptic agents are largely ineffective against its spores)

Alcohol-based hand sanitizers may be used in all other clinical situations if the hands aren’t visibly soiled.

Additional precautions

Make sure mouthpieces, one-way valve masks, resuscitation bags, and other ventilation devices are available in areas where the need for resuscitation is likely. Note: Saliva has not been implicated in human immunodeficiency virus transmission.
If you have any exudative lesions or weeping dermatitis, refrain from direct patient care and from handling patient care equipment until the condition resolves.
Respiratory hygiene/cough etiquette includes covering the mouth and nose with a tissue when coughing and prompt disposal of used tissues, using surgical masks on the coughing person when tolerated, and hand hygiene before and after contact with respiratory secretions.

Although preventive antibiotic therapy may prevent certain diseases, the risk of superinfection and the emergence of drug-resistant strains may outweigh the benefits. Therefore, preventive antibiotics are usually reserved for patients at high risk for exposure to dangerous infections. Antibiotic-resistant bacteria are on the rise mainly because antibiotics have been misused and overused. Some bacteria, such as enterococci, have developed mutant strains that don’t respond to antibiotic therapy.

HEALTH CARE-ASSOCIATED INFECTIONS

A health care-associated infection is an infection that develops as a result of health care. Health care-associated infections were previously known as nosocomial infections, but the name was updated because these infections may be acquired from, or associated with, any portion of the health care-delivery system, including such areas as outpatient care, ambulatory care, home care, or long-term care.

Health care-associated infections are usually transmitted by direct contact. Less commonly, transmission occurs by inhalation or by contact with contaminated equipment and solutions. Contamination of solutions during the manufacturing process is rare.

Despite facility programs of infection control that include surveillance, prevention, and education, about 5% to 10% of patients who enter health care facilities contract a health careassociated infection. Staphylococcal infections, which had been declining since the 1960s, are currently a common cause of infection. Gramnegative bacilli, resistant enterococci, and fungal infections are also on the rise.

Health care-associated infections continue to be a difficult problem, because today’s hospital patients are older and more debilitated with chronic underlying diseases than in the past. Also, the increased use of invasive and surgical procedures, immunosuppressants, and antibiotics predisposes patients to infection and superinfection. At the same time, the growing number of personnel who can come in contact with each patient makes the risk of exposure greater.

The following measures can help prevent health care-associated infections:

Follow strict infection-control procedures. (See Standard precautions. See also CDC isolation precautions, page 802.)

CDC isolation precautions

To help health care facilities maintain up-to-date isolation practices, the Centers for Disease Control and Prevention (CDC) and the Hospital Infection Control Practices Advisory Committee (HICPAC) have developed the Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings. The HICPAC/CDC guidelines contain two tiers of precautions to prevent transmission of infectious agents: standard precautions and transmission-based precautions. In addition, the guidelines also include recommendations for creating a protective environment for allogeneic hematopoietic stem cell (HSCT) patients.

Standard precautions

Standard precautions are designated for the care of all hospital patients regardless of their diagnosis or presumed infection. Standard precautions are the primary strategy for preventing nosocomial infection and take the place of universal precautions. These precautions apply to:

blood
all body fluids, secretions, and excretions— except sweat—regardless of whether or not they contain visible blood
skin that is not intact
mucous membranes

Transmission-based precautions

These precautions are instituted for patients who are known to be, or suspected of being, infected with a highly transmissible infection— one that requires precautions beyond those set forth for standard precautions. There are three types of transmission-based precautions: airborne, droplet, and contact precautions.

Airborne precautions

Airborne precautions are designed to reduce the risk of airborne transmission of infectious agents. Microorganisms carried through the air can be widely dispersed by air currents, making them available for inhalation or deposit on a susceptible host in the same room or at a longer distance from the infected patient if ventilation creates shared air space.

Airborne precautions include special air handling and ventilation procedures to prevent the spread of infection. They also require the use of respiratory protection such as a respirator (the N95 or higher disposable respirator or a powered air-purifying respirator)—in addition to standard precautions—when entering an infected patient’s room.

Droplet precautions

Droplet precautions are designed to reduce the risk of transmitting infectious agents through large-particle (exceeding 5 µm) droplets. Such transmission involves the contact of infectious agents to the conjunctivae or to the nasal or oral mucous membranes of a susceptible person. Large-particle droplets don’t remain in the air and generally travel short distances of 3′ (1 m) or less. They require the use of a surgical mask—in addition to standard precautions—to protect the mucous membranes.

Contact precautions

Contact precautions are designed to reduce the risk of transmitting infectious agents by direct or indirect contact. Direct-contact transmission can occur through patient care activities that require physical contact. Indirect-contact transmission involves a susceptible host coming in contact with a contaminated object, usually inanimate, in the patient’s environment or with items contaminated with the patient’s secretions, excretions, or blood outside of the patient’s environment that may have been removed from the environment without appropriate cleaning and disinfection.

Contact precautions require the use of gloves and a gown—in addition to standard precautions—to avoid contact with the infectious agent. A mask is only required if there’s a chance of splash or splatter of body fluids to the face. Stringent hand-hygiene is also necessary after removal of the protective items.

Protective environment

A protective environment refers to isolation practices designed to decrease the risk of exposure to environmental fungal agents in allogeneic HSCT patients. Environmental controls include high-efficiency particulate air (HEPA) filtration of incoming air, directed room airflow, positive room air pressure relative to the corridor, well-sealed rooms that prevent infiltration of outside air, at least 12 air exchanges per hour, strategies to minimize dust (such as avoiding upholstery and carpet), and prohibiting dried and fresh flowers and potted plants in rooms of HSCT clients. In addition, during periods of construction or renovation, it is advised that severely immunocompromised patients wear a high-efficiency respiratoryprotection device when they are outside the protective environment.

Immunization schedule

Before immunization, ask the parents if the child is receiving corticosteroids or other drugs that suppress the immune response or if he had a recent febrile illness. Obtain a history of allergic responses, especially to antibiotics, eggs, feathers, and past immunizations. Keep in mind that a child who’s at risk for acquired immunodeficiency syndrome or who tests positive for human immunodeficiency virus infection may need special consideration.

After immunization, tell the parents to watch for and report reactions other than local swelling and pain and mild temperature elevation. Give them the child’s immunization record. The following are the 2011 general vaccine recommendations approved by the Advisory Committee on Immunization Practices, the American Academy of Pediatrics, and the American Academy of Family Physicians.

Age	Immunization
Birth	HepB
1 to 4 months	HepB
2 months	DTaP, HIB, IPV, PCV, Rota
4 months	DTaP, HIB, IPV, PCV, Rota
6 months	DTaP, HIB, PCV, Rota
6 to 18 months	HepB, IPV
12 to 15 months	HIB, MMR, PCV, HepA, varicella
6 months to 18 years	Influenza (yearly)
12 to 23 months	HepA
15 to 18 months	DTaP, HepA
4 to 6 years	DTaP, IPV, MMR, varicella
11 to 12 years	HPV, Tdap, MCV4
15 years	Tdap, MCV4

Document hospital infections as they occur.
Identify outbreaks early, and take steps to prevent their spread.
Eliminate unnecessary procedures that contribute to infection.
Strictly follow necessary isolation techniques.
Observe all patients for signs of infection, especially those patients at high risk.
Always follow proper hand-hygiene technique and encourage other staff members to follow these guidelines as well.
Keep staff members and visitors with obvious infection and well-known carriers away from susceptible, high-risk patients.
Take special precautions with vulnerable patients, such as those with indwelling urinary catheters, mechanical ventilators, or I.V. lines and those recovering from surgery.

ACCURATE ASSESSMENT VITAL

Accurate assessment helps identify infectious diseases and prevents avoidable complications. Complete assessment consists of patient history, physical examination, and laboratory data. The history should include the patient’s sex, age, address, occupation, and place of work; known exposure to illness and recent medications, including antibiotics; and date of disease onset. Signs and symptoms, including their duration and whether they occurred suddenly or gradually, should be included in the history as well as precipitating factors, relief measures, and weight loss or gain. Detail information about recent hospitalization, blood transfusions, blood donation denial by the Red Cross or other agencies, recent travel or camping trips, exposure to animals, and vaccinations. (See Immunization schedule.) If applicable, ask about possible exposure to sexually transmitted diseases or about drug abuse. Also, try to determine the patient’s resistance to infectious disease. Ask about usual dietary patterns, unusual fatigue, and any conditions, such as neoplastic disease or alcoholism, that may predispose him to infection. Notice if the patient is listless or uneasy, lacks concentration, or has any obvious abnormality of mood or affect.

In suspected infection, a physical examination must assess the skin, mucous membranes, liver, spleen, and lymph nodes. Check for and make note of the location and type of drainage from any skin lesions. Record skin color, temperature, and turgor; ask if the patient has pruritus. Take his temperature, using the same route consistently, and watch for a fever, which is the best indicator of many infections. (Keep in mind that some patients, such as those who are immunocompromised, are unable to spike a fever.) Note and record the pattern of temperature change and the effect of antipyretics. Be aware that certain analgesics may contain antipyretics. With a high fever, especially in children, watch for seizures.

Check the pulse rate. Infection commonly increases the pulse rate, but some infections, notably typhoid fever and psittacosis, may decrease it. Also observe for increased respiratory rate or a change in mental status. In severe infection or when complications are possible, watch for hypotension, hematuria, oliguria, hepatomegaly, jaundice, bleeding from gums or into joints, and an altered level of consciousness. Obtain laboratory studies and appropriate cultures as ordered.

GRAM-POSITIVE COCCI

Staphylococcal infections

Staphylococci are gram-positive bacteria, either coagulase-negative (Staphylococcus epidermidis) or coagulase-positive (Staphylococcus aureus). Coagulase-negative staphylococci grow abundantly as normal flora on skin, but they can also cause boils, abscesses, and carbuncles. In the upper respiratory tract, they’re usually nonpathogenic but can cause serious infections in some individuals such as those who are immunocompromised. Pathogenic strains of staphylococci are found in many adult carriers— usually on the nasal mucosa, axilla, or groin. Sometimes, carriers shed staphylococci, infecting themselves or other susceptible people. Coagulase-positive staphylococci tend to form pus and cause many different types of infections. (See Comparing staphylococcal infections, pages 806 to 811.)

Methicillin-resistant Staphylococcus aureus infection

Methicillin-resistant Staphylococcus aureus (MRSA) is a type of staphylococci that is resistant to the beta-lactam antibiotics (methicillin, oxacillin, penicillin, and amoxicillin). It is spread easily by direct person-to-person contact. Once limited to large teaching hospitals and tertiary care centers, MRSA infection is now endemic in nursing homes, long-term care facilities, and the community. In addition, community acquired MRSA (CA-MRSA) skin infections have been associated with athletic facilities, dormitories, military barracks, correctional facilities, and day-care centers.

Patients most at risk for MRSA infection include immunosuppressed patients, burn patients, intubated patients, and those with central venous catheters, surgical wounds, or dermatitis. Others at risk include those with prosthetic devices, heart valves, and postoperative wound infections. Other risk factors include prolonged hospital stays, extended therapy with multiple or broad-spectrum antibiotics, and close proximity to those colonized or infected with MRSA. Also at risk are patients with acute endocarditis, bacteremia, cervicitis, meningitis, pericarditis, and pneumonia.

CAUSES AND INCIDENCE

MRSA enters health care facilities through an infected or colonized patient or a colonized health care worker. Although MRSA has been recovered from environmental surfaces, it’s transmitted mainly by health care workers’ hands. Many colonized individuals become silent carriers. The most frequent site of colonization is the anterior nares (25% to 30% of people are colonized in the nares with S. aureus, less than 2% are colonized with MRSA). Other, less common sites are the groin, axilla, and the gut. Typically, MRSA colonization is diagnosed by isolating bacteria from nasal secretions.

In individuals in whom the natural defense system breaks down, such as after an invasive procedure, trauma, or chemotherapy, the normally benign bacteria can invade tissue, proliferate, and cause infection. Today, up to 90% of S. aureus isolates or strains are penicillin resistant, and about 50% of all S. aureus isolates are resistant to methicillin, a penicillin derivative, as well as to nafcillin and oxacillin. These strains may also resist cephalosporins, aminoglycosides, erythromycin, tetracycline, and clindamycin.

MRSA infection has become prevalent with the overuse of antibiotics. Over the years, this overuse has given once-susceptible bacteria the chance to develop defenses against antibiotics. This new capability allows resistant strains to flourish when antibiotics kill their moresensitive cousins.

SIGNS AND SYMPTOMS

MRSA may start as small, red bumps that resemble pimples, boils, or spider bites. They can quickly turn into deep, painful abscesses. The bacteria can remain confined to the skin or they can burrow deep into the body and cause lifethreatening infections in joints, bones, surgical wounds, heart valves, lungs, and the bloodstream.

DIAGNOSIS

MRSA can be cultured from the suspected site with the appropriate method. For example, a wound can be swabbed for culture. Cultures of blood, urine, and sputum specimens will reveal sources of MRSA. Many laboratories use oxacillin disks to check for staphylococcus sensitivity when testing culture specimens; resistance to oxacillin indicates MRSA. In addition, a rapid blood test, Staph SR Assay, can detect certain genes common in MRSA. This test, recently approved by the U.S. Food and Drug Administration (FDA), can provide results in 2 hours.

TREATMENT

To eradicate MRSA colonization in the nares, the physician may order topical mupirocin to be applied inside the nostrils. Other protocols involve combining a topical agent and an oral antibiotic. Most facilities keep patients in isolation until surveillance cultures are negative.

The Centers for Disease Control and Prevention (CDC) recommends incision and drainage as the first-line treatment for mild abscesses. If antibiotics are needed, vancomycin or linezolid are the drugs of choice (see Vancomycinresistant infections). A serious adverse effect (mostly caused by histamine release) is itching, which can progress to anaphylaxis. For serious MRSA infections, an infections disease specialist should be consulted.

Vancomycin-resistant infections

Some Staphylococcus aureus organisms have developed resistance to vancomycin. In some cases, the resistance is considered intermediate-strength resistance and is known as vancomycin intermittent-resistant S. aureus (VISA). Another mutation, vancomycin-resistant S. aureus (VRSA), is fully resistant to vancomycin.

Researchers believe VISA and VRSA enter health care facilities through an infected or colonized patient or a colonized health care worker. They spread through direct contact between the patient and caregiver or between patients. They may also be spread through patient contact with contaminated surfaces.

Patients with laboratory-confirmed VISA or VRSA must be placed in a single room on contact precautions, and the number of health care workers involved in patient care should be limited. Other patients who shared the patient’s room should be checked for VISA or VRSA colonization using an anterior nares culture. (Notify the laboratory to look specifically for S. aureus and to check sensitivity).

People involved in direct care of the patient before the initiation of contact precautions should be interviewed regarding the extent of their interactions. Those with extensive interaction should have an anterior nares culture. The local health department should be notified immediately. Antimicrobial treatment may include an increased dosage of vancomycin (for VISA only) and linezolid, quinupristin and dalfopristin, or a combination of other antimicrobials according to the sensitivity pattern of the organism.

SPECIAL CONSIDERATIONS

People in contact with the patient should perform hand hygiene before and after patient care.
Good hand hygiene is the most effective way to prevent MRSA infection from spreading.
Use an antiseptic soap such as chlorhexidine. Bacteria have been cultured from worker’s hands washed with milder soap. One study showed that, without proper hand hygiene, MRSA could survive on health care workers’ hands for up to 3 hours. Chlorhexidine has a residual antimicrobial effect on the skin.

Comparing staphylococcal infections

Predisposing factors

Signs and symptoms

Diagnosis

Treatment

Special considerations

Bacteremia

Infected surgical wounds

Abscesses

Infected I.V. or intraarterial catheter sites or catheter tips

Infected vascular grafts or prostheses

Infected pressure ulcers

Osteomyelitis

Parenteral drug abuse

Source unknown (primary bacteremia)

Cellulitis

Burns

Immunosuppression

Debilitating diseases, such as chronic renal insufficiency or diabetes

Infective endocarditis (coagulase-positive staphylococci) and subacute bacterial endocarditis (coagulase-negative staphylococci)

Cancer (leukemia) or neutrophil nadir after chemotherapy or radiation

Fever (high fever with no obvious source in children younger than age 1), shaking chills, tachycardia

Cyanosis or pallor

Confusion, agitation, stupor

Skin microabscesses

Joint pain

Complications: sepsis; shock; acute bacterial endocarditis (in prolonged infection; indicated by new or changing systolic murmur); retinal hemorrhages; splinter hemorrhages under nails and small, tender red nodes on pads of fingers and toes (Osler’s nodes); abscess formation in skin, bones, lungs, brain, and kidneys; pulmonary emboli if tricuspid valve is infected

Prognosis depends on early diagnosis and treatment, and presence of other medical conditions

Blood cultures (two to four samples from different sites at different times): growing staphylococci and leukocytosis (usually 12,000 white blood cells [WBCs]/µl), with a shift to the left of polymorphonuclear leukocytes (70% to 90% neutrophils)

Urinalysis may show microscopic hematuria

Erythrocyte sedimentation rate (ESR) elevated, especially in chronic or subacute bacterial endocarditis

Prolonged partial thromboplastin time and prothrombin time; low fibrinogen and platelet counts, and low factor assays; possible disseminated intravascular coagulation

Cultures of urine, sputum, and skin lesions with discharge may identify primary infection site; chest X-rays and scans of lungs, liver, abdomen, and brain may assist with identification

Echocardiogram may show heart valve vegetation

Semisynthetic penicillins (oxacillin, nafcillin) or cephalosporins (cefazolin) given I.V.

Vancomycin I.V. for patients with penicillin allergy or suspected methicillin-resistant organisms

Possibly, probenecid given to partially prevent urinary excretion of penicillin and to prolong blood levels

I.V. fluids to reverse shock

Removal of infected catheter or foreign body

Surgery

Report infection to authorities as required.

S. aureus bacteremia can be fatal within 12 hours. Be especially alert for it in debilitated patients with I.V. catheters or in those with a history of drug abuse.

Administer antibiotics on time to maintain adequate blood levels, but give them slowly, using the prescribed amount of diluent, to prevent thrombophlebitis.

Watch for signs of penicillin allergy, especially pruritic rash (anaphylaxis) and breathing difficulties. Keep epinephrine

1:1,000 and resuscitation equipment handy. Monitor the patient’s vital signs, urine output, and mental state for signs of shock.

Obtain cultures carefully, and observe for clues to the primary site of infection. Never refrigerate blood cultures; it delays identification of organisms by slowing their growth.

If the patient has methicillin-resistant Staphylococcus aureus (MRSA): regardless of site, place patient on contact precautions.

Obtain peak and trough levels of vancomycin to determine the adequacy of treatment.

Administer vancomycin I.V. slowly over 1 hour to avoid any adverse reactions.

Pneumonia

Immune deficiencies, especially in elderly and in children younger than age 2

Chronic lung diseases and cystic fibrosis

Malignant tumors

Antibiotics that kill normal respiratory flora but spare

S. aureus

Viral respiratory infections, especially influenza

Hematogenous (bloodborne) bacteria spread to the lungs from primary sites of infection (such as heart valves, abscesses, and pulmonary emboli)

Recent bronchial or endotracheal suctioning or intubation

High temperature: adults, 103° to 105° F (39.4° to 40.6° C); children, 101° F (38.3° C) or above

Cough, with purulent, yellow, or bloody sputum

Dyspnea, crackles, and decreased breath sounds

Pleuritic pain

In infants: mild respiratory infection that suddenly worsens: irritability, anxiety, dyspnea, anorexia, vomiting, diarrhea, spasms of dry coughing, marked tachypnea, expiratory grunting, sternal retractions, and cyanosis

Complications: necrosis, lung abscess, pyopneumothorax, empyema, pneumatocele, shock, hypotension, pleural effusions, respiratory failure, confusion

WBC count may be elevated (15,000 to 40,000/µl in adults; 15,000 to 20,000/µl in children), with predominance of polymorphonuclear leukocytes

Sputum Gram stain: mostly gram-positive cocci in clusters, with many polymorphonuclear leukocytes

Sputum culture: mostly coagulase-positive staphylococci

Chest X-rays: usually patchy infiltrates

Arterial blood gas analysis: hypoxia and respiratory acidosis

Semisynthetic penicillins (oxacillin, nafcillin) or cephalosporins (cefazolin) given I.V.

Vancomycin I.V. for patients with penicillin allergy or suspected methicillin-resistant organisms

Isolation for MRSA until the patient is off antibiotics and symptoms resolve (some facilities may require negative cultures)

The Centers for Disease Control and Prevention’s isolation guidelines require standard precautions unless MRSA, which requires contact precautions, is present.

Keep the door to the patient’s room closed. Don’t store extra supplies in his room. Disposable suction containers are preferred.

When obtaining sputum specimens, make sure you’re collecting thick sputum, not saliva. The presence of epithelial cells (found in the mouth, not lungs) indicates a poor specimen.

Administer antibiotics strictly on time, but slowly. Watch for signs of penicillin allergy and for signs of infection at the I.V. sites. Change the I.V. site every third day.

Perform frequent chest physical therapy. Do chest percussion and postural drainage after intermittent positive pressure breathing treatments. Concentrate on consolidated areas (revealed by X-rays or auscultation).

Enterocolitis

Broad-spectrum antibiotics (tetracycline, chloramphenicol, or neomycin) or aminoglycosides (tobramycin, streptomycin, or kanamycin) as prophylaxis for bowel surgery or treatment of hepatic coma

Usually occurs in elderly patients, but also in neonates (associated with staphylococcal skin lesions)

Sudden onset of profuse, watery diarrhea usually 2 days to several weeks after start of antibiotic therapy, I.V. or by mouth (P.O.)

Nausea, vomiting, abdominal pain and distention

Hypovolemia and dehydration (decreased skin turgor, hypotension, fever)

Stool Gram stain: many grampositive cocci and polymorphonuclear leukocytes, with few gram-negative rods

Stool culture: S. aureus

Sigmoidoscopy: mucosal ulcerations

Blood studies: leukocytosis, moderately increased blood urea nitrogen level, and decreased serum albumin level

Broad-spectrum antibiotics discontinued

Possibly, antistaphylococcal agents such as vancomycin P.O.

Normal flora replenished with yogurt that contains live cultures

Monitor vital signs frequently to detect early signs of shock.

Force fluids to correct dehydration.

Know serum electrolyte levels. Measure and record bowel movements when possible. Check serum chloride level for alkalosis (hypochloremia). Watch for dehydration and electrolyte imbalance.

Collect serial stool specimens for Gram stain and culture to confirm diagnosis. (The effectiveness of therapy is usually measured by clinical response.)

Observe standard precautions. Use contact precautions for diapered or incontinent children for duration of illness.

Follow reporting requirements, especially in a group situation such as a nursing home. They may vary per facility protocol.

Osteomyelitis

Hematogenous organisms

Skin trauma

Infection spreading from adjacent joint or other infected tissues

S. aureus bacteremia

Orthopedic surgery or trauma

Cardiothoracic surgery

Usually occurs in growing bones, especially femur and tibia, of children younger than age 12

More common in males

Abrupt onset of fever—usually 101° F (38.3° C) or above; shaking chills; pain and swelling over infected area; restlessness; headache

About 20% of children develop a chronic infection if not properly treated

Possible history of prior trauma to involved area

Positive bone and pus cultures (and blood cultures in about 50% of patients)

X-ray changes apparent after second or third week

ESR elevated with leukocyte shift to the left

Surgical debridement

Prolonged antibiotic therapy (4 to 8 weeks)

Vancomycin I.V. for patients with penicillin allergy or methicillin-resistant organisms

Possibly, removal of prosthesis or hardware

Identify the infected area, and mark it on the care plan.

Check the penetration wound from which the organism originated for evidence of present infection.

Severe pain may render the patient immobile. If so, perform passive range-of-motion exercises. Apply heat as needed, and elevate the affected part. (Extensive involvement may require casting until the infection subsides.)

Before procedures such as surgical debridement, warn the patient to expect some pain. Explain that drainage is essential for healing, and that he will continue to receive analgesics and antibiotics after surgery.

Food poisoning

Enterotoxin produced by toxigenic strains of S. aureus in contaminated food (second most common cause of food poisoning in United States)

Anorexia, nausea, vomiting, diarrhea, and abdominal cramps 1 to 6 hours after ingestion of contaminated food

Symptoms usually subside within 18 hours, with complete recovery occuring in 1 to 3 days

Clinical findings sufficient

Stool cultures: usually negative for S. aureus

Epidemiologic history: if others are ill and food history is a commonality; health department may be contacted for an outbreak

No treatment necessary unless dehydration becomes a problem (usually in infants and elderly); oral rehydrating solution or I.V. therapy may be necessary to replace fluids

Monitor vital signs, fluid balance, and serum electrolyte levels.

Check for dehydration if vomiting is severe or prolonged and for decreased blood pressure.

Observe and report the number and color of stools.

Report infection to authorities as required.

Obtain a complete history of symptoms, recent meals, and other known cases of food poisoning.

Skin infections

Decreased resistance

Burns or pressure ulcers Decreased blood flow

Possible skin contamination from nasal discharge

Foreign bodies

Underlying skin diseases, such as eczema and acne

Common in people with poor hygiene living in crowded quarters

Insulin-dependent diabetes mellitus

Hemodialysis

I.V. drug injection

Cellulitis—diffuse, acute inflammation of soft tissue (no discharge)

Pus-producing lesions in and around hair follicles (folliculitis)

Boil-like lesions (furuncles and carbuncles) extend from hair follicles to subcutaneous tissues; these painful, red, indurated lesions are 1 to 2 cm and have a purulent yellow discharge

Small macules or skin blebs that may develop into vesicles containing pus (bullous impetigo); common in school-age children

Mild or spiking fever

Malaise

Clinical findings and analysis of pus cultures if sites are draining

Cultures of nondraining cellulitis taken from the margin of the reddened area by infiltration with 1 mL sterile saline solution (nonbacteriostatic saline) and immediate fluid aspiration

Topical ointments; gentamicin or bacitracin-neomycin polymyxin

P.O. cloxacillin, dicloxa cillin, or erythromycin; I.V. oxacillin or nafcillin for severe infection; I.V. vancomycin for methicillin-resistant organisms

Application of heat to reduce pain

Surgical drainage

Identification and treatment of sources of reinfection (nostrils, perineum)

Cleaning and covering the area with moist, sterile dressings

Identify the site and extent of infection.

Keep lesions clean with saline solution and peroxide irrigations, as ordered. Cover infections near wounds or the genitourinary tract with gauze pads. Keep pressure off the site to facilitate healing.

Be alert for the extension of skin infections.

Severe infection or abscess may require surgical drainage. Explain the procedure to the patient. Determine if cultures will be taken, and be prepared to collect a specimen.

Impetigo is contagious. Isolate the patient and alert his family. Use contact precautions for all draining lesions.

Use contact precautions for duration of illness for major skin/wound infections where there is no dressing or dressing does not adequately contain drainage.

Contact isolation precautions should be used when in contact with the patient. A disinfected private room should be made available with dedicated equipment.
Change gloves when contaminated or when moving from a “dirty” area of the body to a clean one.
Instruct the patient’s family and friends to wear protective clothing when they visit him, and show them how to dispose of it.
Provide teaching and emotional support to the patient and his family members.
Consider grouping infected patients together and having the same nursing staff care for them.
Don’t lay equipment used on the patient on the bed or bed stand. Be sure to wipe it with appropriate disinfectant before leaving the room.
Ensure judicious and careful use of antibiotics. Encourage physicians to limit their use.
Instruct the patient to take antibiotics for the full period prescribed, even if he begins to feel better.

Streptococcal infections

Streptococci are small gram-positive bacteria, spherical to ovoid in shape, and linked together in pairs or chains. Several species occur as part of normal human flora in the respiratory, GI, and genitourinary tracts. Although researchers have identified 21 species of streptococci, three classes—groups A, B, and D—cause most of the infections. (See Comparing streptococcal infections, pages 812 to 817.) Organisms belonging to groups A and B betahemolytic streptococci are associated with a characteristic pattern of human infections. Most disorders due to group D streptococcus are caused by Enterococcus faecalis, formerly called Streptococcus faecalis, or S. bovis. Group C and group G streptococci have been identified as the etiologic agent in such infections as bacteremia, meningitis, pharyngitis, osteomyelitis, and neonatal sepsis.

Clinically, there are three states of streptococcal infection: carrier, acute, and delayed nonsuppurative complications. In the carrier state, the patient is infected with a diseasecausing species of streptococci without evidence of infection. In the acute form, streptococci invade the tissues and cause physical symptoms. In the delayed nonsuppurative complications state, specific signs and symptoms associated with streptococcal infection occur. These include those associated with the inflammatory state of acute rheumatic fever, chorea, and glomerulonephritis. If further complications occur, they usually appear about 2 weeks after the acute illness, but they may be evident after a nonsymptomatic illness.

Necrotizing fasciitis

Most commonly referred to as flesh-eating bacteria, necrotizing fasciitis is a progressive, rapidly spreading inflammatory infection located in the deep fascia that destroys fascia and fat with secondary necrosis of subcutaneous tissue. Also referred to as hemolytic streptococcal gangrene, acute dermal gangrene, suppurative fasciitis, and synergistic necrotizing cellulites, necrotizing fasciitis is most commonly caused by the pathogenic bacteria Streptococcus pyogenes, also known as group A Streptococcus (GAS), although other aerobic and anaerobic pathogens may be present.

This severe and potentially fatal infection may begin at the site of a small insignificant wound or surgical incision. It’s characterized by invasive and progressive necrosis of the soft tissue and underlying blood supply. (See Necrotizing Fasciitis, page 818.) The high mortality rates associated with it have been attributed to the emergence of more virulent strains of streptococci caused by changes in the bacteria’s deoxyribonucleic acid.

This would account for an increase in the frequency and severity of the cases reported since 1985, following a 50- to 60-year span of clinical insignificance. Noted for decades and described in medical literature since the Civil War, necrotizing fasciitis accounts for 8% of reported cases of invasive GAS infections today. The mortality rate is very high, at 70% to 80%. Mortality drops significantly and prognosis improves with early intervention and treatment. Cases treated aggressively with surgery, antibiotics, and hyperbaric oxygen (HBO) therapy have seen mortality rates reduced to as low as 9% to 20%.

CAUSES AND INCIDENCE

More than 80 types of the causative bacteria S. pyrogenes are in existence, making the epidemiology of GAS infections most complex. Wounds as minor as pinpricks, needle punctures, bruises, blisters, and abrasions or as serious as a traumatic injury or surgical incision can provide an opportunity for bacteria to enter the body.

In necrotizing fasciitis, group A beta-hemolytic Streptococcus and Staphylococcus aureus, working alone or together, are most commonly the primary infecting bacteria. They can enter the host via local tissue injury or through a breach in the integrity of a mucous membrane barrier. Other aerobic and anaerobic pathogens, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella, may be present. They can proliferate in an environment of tissue hypoxia caused by trauma, recent surgery, or medical compromise. The end product of this invasion is necrosis of the surrounding tissue, which accelerates the disease process by creating an even more favorable environment for the organisms.

Comparing streptococcal infections

Causes and incidence

Signs and symptoms

Diagnosis

Complications

Treatment and special considerations

Streptococcus pyogenes (Group A streptococcus)

Streptococcal pharyngitis (strep throat)

Accounts for 95% of all cases of bacterial pharyngitis

Most common in children ages 5 to 10, from October to April

Spread by direct person-to-person contact via droplets of saliva or nasal secretions

Organism usually colonizes throats of persons with no symptoms

Up to 20% of school children may be carriers

After 1- to 5-day incubation period: temperature of 101° to 104° F (38.3° to 40° C), sore throat with severe pain on swallowing, beefy red pharynx, tonsillar exudate, edematous tonsils and uvula, swollen glands along the jaw line, generalized malaise and weakness, anorexia, occasional abdominal discomfort

Up to 40% of small children have symptoms too mild for diagnosis

Fever abates in 3 to 5 days; nearly all symptoms subside within a week

Clinically indistinguishable from viral pharyngitis

Throat culture showing group A beta-hemolytic streptococci (carriers have positive throat culture)

Elevated white blood cell (WBC) count

Serology showing a fourfold rise in streptozyme titers during convalescence

Acute otitis media or acute sinusitis occurs most frequently

Rarely, bacteremic spread may cause arthritis, endocarditis, meningitis, osteomyelitis, or liver abscess

Poststreptococcal sequelae: acute rheumatic fever or acute glomerulonephritis

Reye’s syndrome

Penicillin or erythromycin, analgesics, and antipyretics may be ordered.

Stress the need for bed rest and droplet precaution isolation from other children for 24 hours after antibiotic therapy begins; the patient should finish his prescription, even if symptoms subside; abscess, glomerulonephritis, and rheumatic fever can occur.

Tell the patient not to skip doses and to properly dispose of soiled tissues.

Scarlet fever (scarlatina)

Usually follows streptococcal pharyngitis; may follow wound infections or puerperal sepsis

Caused by streptococcal strain that releases an erythrogenic toxin

Most common in children ages 2 to 10

Spread by large respiratory droplets or direct contact with items soiled with respiratory secretions

Streptococcal sore throat, fever, strawberry tongue, fine erythematous rash that blanches on pressure and resembles sunburn with goosebumps

Rash usually appearing first on upper chest, then spreading to neck, abdomen, legs, and arms, sparing soles and palms; flushed cheeks, pallor around mouth

Skin sheds during convalescence

Characteristic rash and strawberry tongue

Culture and Gram stain showing S. pyogenes from nasopharynx

Granulocytosis

Although rare, complications may include high fever, arthritis, jaundice, pneumonia, pericarditis, and peritonsillar abscess

Penicillin or erythromycin may be ordered.

Keep the patient in isolation for the first 24 hours.

Carefully dispose of purulent discharge.

Stress the need for prompt and complete antibiotic treatment.

Erysipelas

Occurs primarily in infants and adults older than age 30

Usually follows streptococcal pharyngitis

Exact mode of spread to skin unknown

Sudden onset, with reddened, swollen, raised lesions (skin looks like an orange peel), usually on face and scalp, bordered by areas that often contain easily ruptured blebs filled with yellow-tinged fluid; lesions sting and itch; lesions on the trunk, arms, or legs usually affect incision or wound sites

Other symptoms: vomiting, fever, headache, cervical lymphadenopathy, sore throat

Typical reddened lesions

Culture taken from edge of lesions showing group A beta-hemolytic streptococci

Throat culture almost always positive for group A beta-hemolytic streptococci

Untreated lesions on trunk, arms, or legs may involve large body areas and lead to death

Penicillin or erythromycin I.V. or by mouth (P.O.) may be ordered.

Cold packs, analgesics (aspirin and codeine for local discomfort), and topical anesthetics may be used to increase comfort.

Prevention includes prompt treatment of streptococcal infections and drainage and secretion precautions.

Impetigo (streptococcal pyoderma)

Common in children ages 2 to S in hot, humid weather; high rate of familial spread

Predisposing factors: close contact in schools, overcrowded living quarters, poor skin hygiene, minor skin trauma

May spread by direct contact, environmental contamination, or arthropod vector

Small macules rapidly develop into vesicles, then become pustular and encrusted, causing pain, surrounding erythema, regional adenitis, cellulitis, and itching; scratching spreads infection

Lesions commonly affect the face, heal slowly, and leave depigmented areas

Characteristic lesions with honey-colored crust

Culture and Gram stain of swabbed lesions showing S. pyogenes

Septicemia (rare)

Ecthyma, a form of impetigo with deep ulcers

Penicillin I.V. or P.O., erythromycin, or antibiotic ointments may be ordered.

Perform frequent washing of lesions with antiseptics, such as povidone-iodine or antibacterial soap, followed by thorough drying.

Isolate a patient with draining wounds, using contact precautions.

Prevention includes good hygiene and proper wound care.

Streptococcus agalactiae (Group B streptococcus)

Neonatal streptococcal infections

Incidence of early-onset infection (age 6 days or younger): 2/1,000 live births

Incidence of late-onset infection (age 7 days to 3 months): 1/1,000 live births

Spread by vaginal delivery or hands of nursery staff

Predisposing factors: maternal genital tract colonization, membrane rupture over 24 hours before delivery, crowded nursery

Early onset: bacteremia, pneumonia, and meningitis; mortality from 14% for infants weighing more than 1,500 g at birth to 61% for infants weighing less than 1,500 g at birth

Late onset: bacteremia with meningitis, fever, and bone and joint involvement; mortality 15% to 20%

Other signs and symptoms, such as skin lesions, depend on the site affected

Isolation of group B streptococcus from blood, cerebrospinal fluid (CSF), or skin

Chest X-ray showing massive infiltrate similar to that of respiratory distress syndrome or pneumonia

Overwhelming pneumonia, sepsis, and death

Penicillin or ampicillin and an aminoglycoside I.V. may be ordered.

Patient isolation is unnecessary unless an open draining lesion is present, but proper hand-hygiene is essential; for a draining lesion, take drainage and secretion precautions.

Group B streptococcus prophylaxis may be ordered for women who are pregnant if vaginal or rectal cultures are positive at 35 to 37 weeks’ gestation or if the patient meets other criteria, such as delivery earlier or later than 3 weeks of term, amniotic fluid rupture for 18 hours or more, or an intrapartum temperature greater than or equal to 100.4° F [38.0° C]).

Adult group B streptococcal infection

Most adult infections occur in postpartum women, usually in the form of endometritis or wound infection following cesarean section

Incidence of group B streptococcal endometritis: 1.3/1,000 live births

Group B streptococcal bacteremia and pneumonia: occur in the elderly and frequently in patients with diabetes

Invasive group B streptococcal infection: occurs in patients with human immunodeficiency virus

Fever, malaise, and uterine tenderness

Change in lochia

Bacteremia and pneumonia patients: can exhibit neurologic symptoms such as a change in mental status

Isolation of group B streptococcus from blood or infection site

Bacteremia followed by meningitis or endocarditis

Ampicillin or penicillin I.V. may be ordered.

Perform careful observation for symptoms of infection following delivery.

Follow drainage and secretion precautions.

Streptococcus pneumoniae

Pneumococcal pneumonia

Accounts for 70% of all cases of bacterial pneumonia

More common in men, elderly, Blacks, and Native Americans, in winter and early spring

Spread by droplets and contact with infective secretions

Predisposing factors: trauma, viral infection, underlying pulmonary disease, overcrowded living quarters, chronic diseases, asplenia, and immunodeficiency

Among the 10 leading causes of death in the United States

Sudden onset with severe shaking chills, temperature of 102° to 105° F (38.9° to 40.6° C), bacteremia, cough (with thick, scanty, blood-tinged sputum) accompanied by pleuritic pain

Malaise, weakness, and prostration common

Tachypnea, anorexia, nausea, and vomiting less common

Severity of pneumonia usually caused by host’s cellular defenses, not bacterial virulence

Gram stain of sputum showing gram-positive diplococci; culture showing S. pneumoniae

Chest X-ray showing lobular consolidation in adults; bronchopneumonia in children and elderly patient

Elevated WBC count

Blood cultures usually positive for S. pneumoniae

Pleural effusion (occurs in 25% of patients)

Pericarditis (rare)

Lung abscess (rare)

Bacteremia

Disseminated intravascular coagulation

Death possible if bacteremia is present

Penicillin or erythromycin I.V. or I.M. may be ordered.

Monitor and support respirations, as needed.

Record sputum color and amount.

Prevent dehydration.

Avoid sedatives and opioids to preserve cough reflex.

Carefully dispose of all purulent drainage (standard precautions); advise high-risk patients to receive a vaccine and to avoid infected people.

Otitis media

High incidence, with about 76% to 95% of all children having otitis media at least once (S. pneumoniae causes half of these cases.)

Ear pain, ear drainage, hearing loss, fever, lethargy, and irritability

Other possible symptoms: vertigo, nystagmus, and tinnitus

Fluid in middle ear

Isolation of S. pneumoniae from aspirated fluid if necessary

Recurrent attacks (may cause hearing loss)

Amoxicillin or ampicillin and analgesics may be ordered.

Tell the patient to report a lack of response to therapy after 72 hours.

Meningitis

Can follow bacteremic pneumonia, mastoiditis, sinusitis, skull fracture, or endocarditis

Mortality (30% to 60%) highest in infants and elderly people

Fever, headache, nuchal rigidity, vomiting, photophobia, lethargy, coma, wide pulse pressure, and bradycardia

Isolation of S. pneumoniae from CSF or blood culture

Increased CSF cell count and protein level; decreased CSF glucose level

Computed tomography scan of head

EEG

Persistent hearing deficits, seizures, hemiparesis, or other nerve deficits

Encephalitis

Penicillin I.V. or chloramphenicol may be ordered.

Monitor the patient closely for neurologic changes.

Watch for symptoms of septic shock, such as acidosis and tissue hypoxia.

Group D streptococcus

Endocarditis

Group D streptococcus (enterococcus): causes 10% to 20% of all bacterial endocarditis

Most common in elderly people and in those who abuse I.V. substances

Typically follows bacteremia from an obvious source, such as a wound infection, urinary tract infection, or I.V. insertion site infection

Most cases are subacute

Also causes urinary tract infection

Weakness, fatigability, weight loss, fever, night sweats, anorexia, arthralgia, splenomegaly, and new systolic murmur

Anemia, increased erythrocyte sedimentation rate and serum immuno-globulin level, and positive blood culture for group D streptococcus

Echocardiogram showing vegetation on valves

Embolization

Pulmonary infarction

Osteomyelitis

Penicillin for Streptococcus bovis (non-enterococcal group D streptococcus) may be ordered.

Penicillin or ampicillin and an aminoglycoside for enterococcal group D streptococcus may be ordered.

Men are three times more likely to develop this rare condition than women, and the disease rarely occurs in children except in countries with poor hygienic practices. The mean age of the population contracting the disease is 38 to 44 years.

SIGNS AND SYMPTOMS

Pain, out of proportion to the size of the wound or injury it’s associated with, is usually the first symptom of necrotizing fasciitis. It generally presents before all other physical findings.

The infective process will usually begin with a mild area of erythema at the site of insult, which will quickly progress within the first 24 hours. During the first 24- to 48-hour period, the erythema changes from red to purple and then to blue, with the formation of fluid-filled blisters and bullae that indicate the rapid progression of the necrotizing process. By days 4 and 5, multiple patches of this erythema form, producing large areas of gangrenous skin. By days 7 to 10, dead skin begins to separate at the margins of the erythema, revealing extensive necrosis of the subcutaneous tissue. At this stage, fascial necrosis is typically more advanced than appearance would suggest.

Other clinical symptoms include fever and hypovolemia. In later stages, hypotension and respiratory insufficiency, which are signs of overwhelming sepsis requiring supportive care, occur. In the most severe cases, necrosis advances rapidly until several large areas of the body are involved. This may cause the patient to become mentally cloudy, delirious, or even unresponsive secondary to the intoxication rendered.

Other complications include renal failure, septic shock with cardiovascular collapse, and scarring with cosmetic deformities. Without treatment, involvement of deeper muscle layers may occur, resulting in myositis or myonecrosis.

DIAGNOSIS

Tissue biopsy is the best method of diagnosing necrotizing fasciitis. Cultures of microorganisms can be obtained locally from the periphery of the spreading infection or from deeper tissues during surgical debridement. Gram stain and culturing of biopsied tissue are useful in establishing the type of invasive organisms and the effective treatment against them.

Radiographic studies can pinpoint the presence of subcutaneous gases, and computed tomography scans can locate the anatomic site of involvement by locating the necrosis. In combination with clinical assessment, magnetic resonance imaging determines areas of necrosis and the need for surgical debridement.

Other supportive studies include laboratory values such as complete blood count with differential, electrolytes, glucose, blood urea nitrogen and creatinine, urinalysis, and arterial blood gas levels.

Other conditions to consider in the differential diagnosis include cellulitis, testicular torsion, epididymitis and orchitis (as related to Fournier’s gangrene), gas gangrene, hernias, and toxic shock syndrome (TSS).

TREATMENT

Prompt and aggressive exploration and debridement of suspected necrotizing fasciitis is mandatory for early, definitive diagnosis and to improve prognosis. Ninety percent of patients who present with clinical signs and symptoms will need immediate surgical debridement, fasciotomy, or amputation.

Penicillin, clindamycin, metronidazole, ceftriaxone, gentamicin, chloramphenicol, and ampicillin are among the medications given orally, I.V., or I.M. to treat the organisms involved with necrotizing fasciitis. The specific drug is determined by the sensitivity of the cultured organisms. When the infection is polymicrobial, medications must be used in combination. Recommendations for specific drugs continue to change as new antibiotics are developed and new resistance emerges.

Reports suggest that the use of HBO therapy decreases the mortality rate, significantly improves the tissues’ defense against infection, and prevents the necrosis from spreading by increasing the normal oxygen saturations of infected wounds by a 1000-fold, causing a bactericidal effect. Typical treatment involves aggressively starting HBO therapy after the first surgical debridement and continuing for a total of 10 to 15 sessions.

SPECIAL CONSIDERATIONS

Antibiotic therapy should be initiated immediately.
Accurate and frequent assessment of the patient’s pain level, mental status, wound status, and vital signs is essential in order to recognize the progression of the wound changes or the development of new signs and symptoms. Changes must be reported and documented immediately.
The need for supportive care, such as endotracheal intubation, cardiac monitoring, fluid replacement, and supplemental oxygen, should be assessed and provided as warranted.
Care of postoperative patients and patients with trauma wounds requires strict sterile technique, good hand hygiene, and barriers between health care providers and patients to prevent contamination.
Use contact precautions for draining wounds for 24 hours after beginning appropriate antibiotic therapy. Use droplet precautions, especially for bedside wound debridement. Outbreaks of serious invasive disease have occurred secondary to transmission among patients and health care workers.
Health care workers with sore throats should see their physician to determine if they have a streptococcal infection. If they are diagnosed positive, they shouldn’t return to work until 24 hours after the initiation of antibiotic therapy.
Risk factors for contracting necrotizing fasciitis include patients with advanced age, human immunodeficiency virus infection, history of alcohol abuse, and varicellar infection. Patients with chronic illnesses, such as cancer, diabetes, cardiopulmonary disease, and kidney disease requiring hemodialysis, as well as those using steroids are more susceptible to GAS infection due to their debilitated immune response.

Vancomycin intermittent-resistant Staphylococcus aureus

Vancomycin intermittent-resistant Staphylococcus aureus (VISA) is a mutation of a bacterium that’s easily spread by direct person-to-person contact. It was first discovered in mid-1996 in a Japanese infant’s surgical wound; similar isolates were later reported in Michigan and New Jersey. The U.S. patients had received multiple courses of vancomycin for methicillin-resistant S. aureus infections.

Another mutation, vancomycin-resistant S. aureus (VRSA), is fully resistant to vancomycin.

CAUSES AND INCIDENCE

VISA or VRSA enters a health care facility through an infected or colonized (symptomfree but infected) patient or colonized health care worker. It’s spread during direct contact between the patient and caregiver or patient-topatient. It may also be spread through patient contact with contaminated surfaces, such as an overbed table. It’s able to live for weeks on surfaces. It has been detected on patient gowns, bed linens, and handrails.

A colonized patient is more than 10 times as likely to become infected with the organism, such as through a breach in the immune system. Patients most at risk for infection include immunosuppressed patients or those with severe underlying disease; patients with a history of taking vancomycin, third-generation cephalosporins, or antibiotics targeted at anaerobic bacteria (such as Clostridium difficile); patients with indwelling urinary or central venous catheters; elderly patients, especially those with prolonged or repeated facility admissions; patients with malignancies or chronic renal failure; patients undergoing cardiothoracic or intra-abdominal surgery or organ transplants; patients with wounds with an opening to the pelvic or intra-abdominal area, such as surgical wounds, burns, and pressure ulcers; patients with enterococcal bacteremia, often associated with endocarditis; and patients exposed to contaminated equipment or to a patient with the infecting microbe.

SIGNS AND SYMPTOMS

The carrier patient is commonly asymptomatic but may have signs and symptoms related to the primary diagnosis. Depending on the source of the infection and the reason for treatment, the patient may exhibit cardiac, respiratory, or other major symptoms. Assessment should focus on the affected body system.

TREATMENT

Because no single antibiotic to combat VISA or VRSA is currently available, the physician may opt not to treat an infection at all. Instead, he may stop all antibiotics and wait for normal bacteria to repopulate and replace the strain. Combinations of various drugs may also be used, depending on the source of the infection.

To prevent the spread of VISA and VRSA, some hospitals perform weekly surveillance cultures on at-risk patients in intensive care units or oncology units and those transferred from a long-term care facility. Any colonized patient is then placed in contact isolation until his culture is negative or he’s discharged. Colonization can last indefinitely; no protocol has been established for the length of time a patient should remain in isolation.

The Centers for Disease Control and Prevention (CDC) and the Hospital Infection Control Practices Advisory Committee implemented a two-level system of precautions to simplify isolation for resistant organisms. The first level calls for standard precautions. The second level calls for transmission-based precautions, implemented when a particular infection is suspected.

SPECIAL CONSIDERATIONS

Wash your hands before and after providing patient care. Good hand washing is the most effective way to prevent VISA and VRSA from spreading. Use an antiseptic soap such as chlorhexidine; bacteria have been cultured from workers’ hands after washing with milder soap.
Minimize the number of staff caring for the patient.
Contact isolation precautions should be used when in contact with the patient. A private room should be used. Use dedicated equipment and disinfect the environment.
Change gloves when contaminated or when moving from a soiled area of the body to a clean one.
Wear mask/eye protection or a face shield when performing splash-generating activities, such as suctioning.
Don’t touch potentially contaminated surfaces, such as a bed or bed stand, after removing gown and gloves.
Be particularly cautious in caring for a patient with an ileostomy, colostomy, or draining wound that isn’t contained by a dressing.
Equipment used on the patient shouldn’t be laid on the bed or bed stand and should be wiped with appropriate disinfectant before leaving the room.
Ensure judicious and careful use of antibiotics. Encourage physicians to limit the use of antibiotics.
Instruct family and friends to wear protective garb when they visit the patient. Demonstrate how to dispose of it.
Provide teaching and emotional support to the patient and his family members.
Instruct the patient to take antibiotics for the full prescription period, even if he begins to feel better.
Contact public health authorities before transfer or discharge.

Vancomycin-resistant enterococcus infection

Vancomycin-resistant enterococcus (VRE) is a mutation of a common bacterium normally found in the GI tract that’s spread easily by direct person-to-person contact. Facilities in more than 40 states have reported VRE infection, with 30% of enterococcus infections in intensive care units (ICUs) and 25% of enterococcus infections in non-ICU areas reporting as vancomycinresistant.

Patients most at risk for VRE infection include:

immunosuppressed patients or those with severe underlying disease
patients with a history of taking vancomycin, third-generation cephalosporins, antibiotics targeted at anaerobic bacteria (such as Clostridium difficile), or multiple courses of antibiotics
patients with indwelling urinary or central venous catheters
elderly patients, especially those with prolonged or repeated hospital admissions
patients with cancer or chronic renal failure
patients undergoing cardiothoracic or intraabdominal surgery or organ transplant
patients with wounds opening into the pelvic or intra-abdominal area, including surgical wounds, burns, and pressure ulcers
patients with enterococcal bacteremia, typically associated with endocarditis
patients exposed to contaminated equipment or to another VRE-positive patient

CAUSES AND INCIDENCE

VRE enters health care facilities through an infected or colonized patient or a colonized health care worker. It can also develop following treatment with vancomycin. VRE spreads through direct contact between the patient and caregiver or between patients. It can also spread through patient contact with contaminated surfaces such as an overbed table, where it’s capable of living for weeks. VRE has also been detected on patient gowns, bed linens, and handrails.

SIGNS AND SYMPTOMS

There are no specific signs and symptoms related to VRE infection. The causative agent may be found incidentally with culture results.

TREATMENT

New antimicrobials, such as linezolid and quinupristin with dalfopristin, are available for treatment of VRE infection. Patients who are already colonized with VRE usually aren’t treated with antimicrobials. Instead, the physician may stop all antibiotics and simply wait for normal bacteria to repopulate and replace the VRE strain. Combinations of various drugs may also be used, depending on the source of the infection.

To prevent the spread of VRE, some facilities perform weekly surveillance cultures on at-risk patients in the intensive care or oncology units and on patients who have been transferred from a long-term care facility. Any colonized patient is then placed in contact isolation until culturenegative or until discharged. Colonization can last indefinitely; no protocol has been established for the length of time a patient should remain in isolation.

SPECIAL CONSIDERATIONS

Hand hygiene before and after care of the patient is crucial. Good hand hygiene is the most effective way to prevent VRE from spreading. Use an antiseptic soap such as chlorhexidine. Bacteria have been cultured from workers’ hands after they’ve washed with milder soap. Alcohol-based hand sanitizers are effective as well.
Use contact precautions when in contact with the patient or his support equipment. Provide the patient with a private room and dedicated equipment. Disinfect the environment and the equipment frequently.
Change gloves when contaminated or when moving from a “dirty” area of the body to a clean one.
Don’t touch potentially contaminated surfaces such as an overbed table after removing your gown and gloves.
Be particularly prudent in caring for a patient with an ileostomy, colostomy, or draining wound that isn’t contained by a dressing.
Instruct the patient’s family and friends to wear protective garb when they visit him, and teach them how to dispose of it. Instruct them on proper hand hygiene.
Provide teaching and emotional support to the patient and his family members.
Consider grouping (“cohorting”) infected or colonized patients together and assigning the same nursing staff to them.
Don’t lay equipment used on the patient on the bed or on the overbed table. Wipe the equipment with the appropriate disinfectant before leaving the room.
Ensure judicious and careful use of antibiotics. Encourage physicians to limit their use.
Instruct patients to take antibiotics for the full period prescribed, even if they begin to feel better.
Report to public health authorities.

Scarlet fever

Although scarlet fever (scarlatina) usually follows streptococcal pharyngitis, it may also occur after other streptococcal infections, such as wound infections, urosepsis, and puerperal sepsis. It’s most common in children ages 3 to 15. The incubation period commonly lasts from 2 to 4 days, but may be only 1 day or extend to 7 days.

CAUSES AND INCIDENCE

Group A beta-hemolytic streptococci cause scarlet fever. The infecting strain produces one of three erythrogenic toxins, which triggers a sensitivity reaction in the patient.

SIGNS AND SYMPTOMS

The patient may report a sore throat, headache, chills, anorexia, abdominal pain, and malaise. He’s likely to have a temperature of 101° to 103° F (38.3° to 39.4° C). In addition, he commonly has had contact with a person with a sore throat.

Inspection of the patient’s mouth initially shows an inflamed and heavily coated tongue. As the disease progresses, note a strawberrylike tongue. As it progresses further, the tongue begins to peel and becomes beefy red. It returns to normal by the end of the second week. The uvula, tonsils, and posterior oropharynx appear red and edematous, with mucopurulent exudate.

Inspection of the skin may reveal a fine, erythematous rash that appears first on the upper chest and back. It later spreads to the neck, abdomen, legs, and arms but doesn’t appear on the soles and palms. The rash resembles sunburn with goose bumps and blanches when pressure is applied. The patient’s face appears flushed, except around the mouth, which remains pale. During convalescence, desquamation of the skin occurs at the tips of the fingers and toes and, occasionally, over wide areas of the trunk and limbs. It’s more pronounced where the erythematous rash was most severe.

The cervical lymph nodes feel enlarged and tender on palpation. The liver may also feel slightly enlarged and tender, and tachycardia may be noted.

SPECIAL CONSIDERATIONS

Implement droplet precautions for 24 hours after starting antibiotic therapy.
Keep the patient on complete bed rest while he’s febrile to prevent complications, promote recovery, and help conserve his energy.
Offer frequent oral fluids and oral hygiene and give antipyretics as ordered.
Apply topical anesthetics on the patient’s tongue and throat to relieve pain.
Provide skin care to relieve discomfort from the rash.
Instruct the patient (or his parents) to make sure he takes his oral antibiotics for the prescribed length of time.

GRAM-NEGATIVE COCCI

Meningococcal infections

Two major meningococcal infections (meningitis and meningococcemia) are caused by the gram-negative bacteria Neisseria meningitidis, which also causes primary pneumonia, purulent conjunctivitis, endocarditis, sinusitis, and genital infection. Meningococcemia occurs as simple bacteremia, fulminating meningococcemia and, rarely, chronic meningococcemia. It commonly accompanies meningitis. (See “Meningitis,” page 180.) Meningococcal infections may occur sporadically or in epidemics; particularly virulent infections may be fatal within a matter of hours.

CAUSES AND INCIDENCE

Meningococcal infections usually occur among children (ages 6 months to 2 years) and men, usually military recruits or those enrolled at institutions, such as colleges, because of overcrowding.

N. meningitidis has seven serogroups (A, B, C, D, X, Y, and Z); group A causes most epidemics. Transmission takes place through inhalation of an infected droplet from a carrier (an estimated 2% to 38% of the population). The bacteria localize in the nasopharynx. After incubating about 3 to 4 days, they spread through the bloodstream to joints, skin, adrenal glands, lungs, and the central nervous system. The tissue damage that results (possibly due to the effects of bacterial endotoxins) produces symptoms and, in fulminating meningococcemia and meningococcal bacteremia, hemorrhage, thrombosis, and necrosis.

SIGNS AND SYMPTOMS

Features of meningococcal bacteremia include sudden spiking fever, headache, sore throat, cough, chills, myalgia (in back and legs), arthralgia, tachycardia, tachypnea, mild hypotension, and a petechial, nodular, or maculopapular rash. Headache and stiff neck can also occur as the infection extends to the meninges.

In about 10% to 20% of patients, the disease progresses to fulminating meningococcemia, with extreme prostration, enlargement of skin lesions, DIC, and shock. Without prompt treatment, death from respiratory or heart failure occurs in 6 to 24 hours.

Characteristics of the rare chronic meningococcemia include intermittent fever, rash, joint pain, and an enlarged spleen.

DIAGNOSIS

Tests that support the diagnosis include counterimmunoelectrophoresis of CSF or blood, low white blood cell count and, in patients with skin or adrenal hemorrhages, decreased platelet and clotting levels. Diagnostic evaluation must rule out Rocky Mountain spotted fever and vascular purpuras.

TREATMENT

As soon as meningococcal infection is suspected, treatment begins with high doses of aqueous penicillin G, ampicillin, or cephalosporins such as ceftriaxone; or, for the patient who is allergic to penicillin, I.V. chloramphenicol. Therapy may also include mannitol for cerebral edema, I.V. heparin for DIC, dopamine for shock, and digoxin and a diuretic if heart failure develops. Supportive measures include fluid and electrolyte maintenance, ventilation (maintenance of a patent airway and oxygen, if necessary), insertion of an arterial or central venous pressure (CVP) line to monitor cardiovascular status, and bed rest.

Prophylaxis with ciprofloxacin or rifampin aids health care personnel who work in close contact with the patient, such as those administering cardiopulmonary resuscitation or assisting with intubation or suctioning without wearing a surgical mask. In addition, anyone who has come into contact with the infected person, including family or child care providers, may need prophylactic antibiotics.

SPECIAL CONSIDERATIONS

Give I.V. antibiotics, as ordered, to maintain blood and CSF drug levels.
Enforce bed rest in early stages. Provide a dark, quiet, restful environment.
Maintain adequate ventilation with oxygen or a ventilator, if necessary. Suction and turn the patient frequently.
Keep accurate intake and output records to maintain proper fluid and electrolyte levels. Monitor blood pressure, pulse, arterial blood gas levels, and CVP.
Watch for complications, such as DIC, arthritis, endocarditis, and pneumonia.
If the patient is receiving chloramphenicol, monitor complete blood count.
Check the patient’s drug history for allergies before giving antibiotics.

To prevent the infection’s spread:

Impose droplet precautions until the patient has had antibiotic therapy for 24 hours.
Label all meningococcal specimens. Deliver them to the laboratory quickly because meningococci are very sensitive to changes in humidity and temperature.
Report all meningococcal infections to public health department officials.

GRAM-POSITIVE BACILLI

Diphtheria

Diphtheria is an acute, highly contagious toxinmediated infection caused by Corynebacterium diphtheriae, a gram-positive rod that usually infects the respiratory tract, primarily the tonsils, nasopharynx, and larynx. The GI and urinary tracts, conjunctivae, and ears are rarely involved.

CAUSES AND INCIDENCE

Transmission usually occurs through intimate contact or by airborne respiratory droplets from asymptomatic carriers or convalescing patients. Many more people carry this disease than contract active infection. Diphtheria is more prevalent during the colder months because of closer person-to-person indoor contact; however, it may be contracted at any time during the year.

Thanks to effective immunization, diphtheria is rare in many parts of the world, including the United States, where there has not been a reported case of respiratory diphtheria since 2004.

SIGNS AND SYMPTOMS

Most infections go unrecognized, especially in partially immunized individuals. After an incubation period of less than a week, clinical cases of diphtheria characteristically show a thick, patchy, grayish green membrane over the mucous membranes of the pharynx, larynx, tonsils, soft palate, and nose; fever; sore throat; and a rasping cough, hoarseness, and other symptoms similar to croup. Attempts to remove the membrane usually cause bleeding, which is highly characteristic of diphtheria. If this membrane causes airway obstruction (particularly likely in laryngeal diphtheria), symptoms include tachypnea, stridor, possibly cyanosis, suprasternal retractions, and suffocation, if untreated. Adenopathy and cervical swelling can occur. In cutaneous diphtheria, skin lesions resemble impetigo.

SPECIAL CONSIDERATIONS

Diphtheria requires comprehensive supportive care with psychological support.

To prevent the spread of this disease, stress the need for droplet precautions. Teach proper disposal of nasopharyngeal secretions. Maintain infection precautions until after two consecutive negative nasopharyngeal cultures—at least 1 week after discontinuing drug therapy. Treatment of exposed individuals with antitoxin remains controversial. Suggest that the patient’s family receive diphtheria toxoid if they haven’t been immunized.
Give drugs as ordered. Although timeconsuming and risky, desensitization should be attempted if tests are positive, because diphtheria antitoxin is the only specific treatment available. If sensitivity tests are negative, the antitoxin is given before laboratory confirmation, because mortality increases directly with any delay in antitoxin administration. Before giving diphtheria antitoxin, which is made from horse serum, obtain eye and skin tests to determine sensitivity. After giving antitoxin or penicillin, be alert for anaphylaxis; keep epinephrine 1:1,000 and resuscitation equipment handy. In patients who receive erythromycin, watch for thrombophlebitis.
Monitor respirations carefully, especially in laryngeal diphtheria (usually, such patients are in a high-humidity environment). Watch for signs of airway obstruction, and be ready to give immediate life support, including intubation and tracheotomy.
Watch for signs of shock, which can develop suddenly.
Obtain cultures as ordered.
If neuritis develops, tell the patient it’s usually transient. Be aware that peripheral neuritis may not develop until 2 to 3 months after the onset of illness.

Report all cases to public health authorities.

Listeriosis

Listeriosis is an infection caused by the weakly hemolytic, gram-positive bacillus Listeria monocytogenes. It occurs most commonly in fetuses, in neonates (during the first 3 weeks of life), and in older or immunosuppressed adults. The infected fetus is usually stillborn or is born prematurely, almost always with lethal listeriosis. This infection produces milder illness in pregnant women and varying degrees of illness in older and immunosuppressed patients; their prognoses depend on the severity of underlying illness.

CAUSES AND INCIDENCE

The primary method of person-to-person transmission is neonatal infection in utero (through the placenta) or during passage through an infected birth canal. Other modes of transmission may include inhaling contaminated dust; drinking contaminated, unpasteurized milk; eating unprocessed soft cheese or deli meats; coming in contact with infected animals, contaminated sewage or mud, or soil contaminated with feces containing L. monocytogenes; and, possibly, person-to-person transmission.

SIGNS AND SYMPTOMS

Contact with L. monocytogenes commonly causes a transient asymptomatic carrier state. But sometimes it produces bacteremia and a febrile, generalized illness. In a pregnant woman, especially during the third trimester, listeriosis causes a mild illness with malaise, chills, fever, and back pain. However, a severe uterine infection may produce abortion, premature delivery, or stillbirth. Transplacental infection may also cause early neonatal death or granulomatosis infantiseptica, which produces organ abscesses in infants.

Infection with L. monocytogenes commonly causes meningitis (especially in immunocompromised patients), resulting in tense fontanels, irritability, lethargy, seizures, and coma in neonates and low-grade fever and personality changes in adults. Fulminant manifestations with coma are rare.

SPECIAL CONSIDERATIONS

Deliver specimens to the laboratory promptly. Because few organisms may be present, take at least 10 ml of spinal fluid for culture.
Use standard precautions until a series of cultures are negative. Be especially careful when handling lochia from an infected mother and secretions from her infant’s eyes, nose, mouth, and rectum, including meconium.
Evaluate neurologic status at least every 2 hours. In an infant, check fontanels for bulging. Maintain adequate I.V. fluid intake; measure intake and output accurately.
If the patient has central nervous system depression and becomes apneic, provide respiratory assistance, monitor respirations, and obtain frequent arterial blood gas measurements.
Provide adequate nutrition by total parenteral nutrition, nasogastric tube feedings, or a soft diet, as ordered.
Allow the patient’s parents to see and, if possible, hold their infant in the neonatal intensive care unit. Be flexible about visiting privileges. Keep the parents informed of the infant’s status and prognosis at all times.
Reassure the parents of an infected neonate who may feel guilty about the infant’s illness.
Report all cases to public health authorities.

To avoid infection, instruct the patient and his family to avoid soft cheeses and to cook such foods as hot dogs thoroughly. Immunocompromised patients should avoid soft cheeses and deli meats.

Tetanus

Tetanus, also known as lockjaw, is an acute exotoxin-mediated infection caused by the anaerobic, spore-forming, gram-positive bacillus Clostridium tetani. This infection is usually systemic; less commonly, it is localized. Tetanus is fatal in up to 60% of unimmunized people, usually within 10 days of onset. When symptoms develop within 3 days after exposure, the prognosis is poor.

CAUSES AND INCIDENCE

Normally, transmission occurs through a puncture wound that’s contaminated by soil, dust, or animal excreta containing C. tetani or by way of burns and minor wounds. After C. tetani enters the body, it causes local infection and tissue necrosis. It also produces toxins that then enter the bloodstream and lymphatics and eventually spread to central nervous system tissue.

Tetanus occurs worldwide, but is more prevalent in agricultural regions and developing countries that lack mass immunization programs. It’s one of the most common causes of neonatal deaths in developing countries, where infants of unimmunized mothers are delivered under unsterile conditions. In such infants, the unhealed umbilical cord is the portal of entry.

In the United States, about 75% of all cases occur between April and September.

SIGNS AND SYMPTOMS

The incubation period varies from 3 to 4 weeks in mild tetanus to under 2 days in severe tetanus. When symptoms occur within 3 days after injury, death is more likely. If tetanus remains localized, signs of onset are spasm and increased muscle tone near the wound.

If tetanus is generalized (systemic), indications include marked muscle hypertonicity, hyperactive deep tendon reflexes, tachycardia, profuse sweating, low-grade fever, and painful, involuntary muscle contractions:

neck and facial muscles, especially cheek muscles—locked jaw (trismus), painful spasms of masticatory muscles, difficulty opening the mouth, and risus sardonicus, a grotesque, grinning expression produced by spasm of facial muscles
somatic muscles—arched-back rigidity (opisthotonos); boardlike abdominal rigidity
intermittent tonic seizures lasting several minutes, which may result in cyanosis and sudden death by asphyxiation

Despite such pronounced neuromuscular symptoms, cerebral and sensory functions remain normal. Complications can include atelectasis, pneumonia, pulmonary emboli, acute gastric ulcers, flexion contractures, and cardiac arrhythmias.

Neonatal tetanus is always generalized. The first clinical sign is difficulty in sucking, which usually appears 3 to 10 days after birth. It progresses to total inability to suck with excessive crying, irritability, and nuchal rigidity.

TREATMENT

Within 72 hours after a puncture wound, a patient with no previous history of tetanus immunization first requires tetanus immune globulin (TIG) or tetanus antitoxin to neutralize the toxins and to confer temporary protection. Next, he needs active immunization with tetanus toxoid. If he hasn’t received tetanus immunization within 10 years, a booster injection of tetanus toxoid is necessary. If tetanus develops despite immediate postinjury treatment, the patient will require airway maintenance and a muscle relaxant, such as diazepam, to decrease muscle rigidity and spasm. If muscle contractions aren’t relieved by muscle relaxants, a neuromuscular blocker may be prescribed. The patient with tetanus needs high-dose antibiotics (penicillin administered I.V. if he isn’t allergic to it or such alternatives as clindamycin, erythromycin, and metronidazole). The source of the toxin needs to be removed and destroyed through surgical exploration and wound debridement.

SPECIAL CONSIDERATIONS

Thoroughly debride and clean the injury site, and check the patient’s immunization history. Record the cause of injury. If it’s an animal bite, report the case to local public health authorities.
Before giving penicillin and TIG, antitoxin, or toxoid, obtain an accurate history of allergies to immunizations or penicillin. If the patient has a history of allergies, keep epinephrine 1:1,000 and resuscitation equipment available.
Stress the importance of maintaining active immunization with a booster dose of tetanus toxoid every 10 years.

After tetanus develops:

Maintain an adequate airway and ventilation to prevent pneumonia and atelectasis. Suction often and watch for signs of respiratory distress. Keep emergency airway equipment on hand because the patient may require artificial ventilation or oxygen administration.
Maintain an I.V. line for medications and emergency care, if necessary.
Monitor the electrocardiogram frequently for arrhythmias. Record intake and output accurately, and check vital signs often.
Turn the patient frequently to prevent pressure ulcers and pulmonary stasis.
Because even minimal external stimulation provokes muscle spasms, keep the patient’s room quiet and only dimly lighted. Warn visitors not to upset or overly stimulate the patient.
If urine retention develops, insert an indwelling urinary catheter.
Give muscle relaxants and sedatives, as ordered, and schedule patient care—such as passive range-of-motion exercises—to coincide with periods of heaviest sedation.

PREVENTION Preventing tetanus

Tetanus can be easily prevented through immunization against the toxin. Almost all cases of tetanus occur in people who’ve never been immunized or who haven’t had a tetanus booster shot within the past 10 years. Having had a tetanus infection doesn’t provide immunity. Following recommendations for vaccinations is necessary to prevent recurrence of tetanus.

The tetanus vaccine is usually given to children as part of the diphtheria and tetanus toxoids and pertussis (DTP) shot.

It’s recommended that adolescents get a booster shot between ages 11 and 18, and that adults receive a routine tetanus booster shot every 10 years. In the event of a deep or dirty wound that occurs when more than 5 years have passed since the last booster shot, it is recommended that another booster be given. Tell your patient to follow these guidelines to help prevent tetanus infection.

Take care of a wound

Tell the patient to do the following:

Rinse the wound thoroughly with clean water.
Clean the wound and the area around it with soap and a washcloth.
Contact a practitioner if debris is embedded in the wound.

Consider the wound source

Tell the patient to contact a practitioner if the wound is deep, especially if it’s dirty or is a result of an animal bite.
Tell the patient to contact a practitioner if the date of his most recent tetanus shot is uncertain.

Use antibiotic ointment or cream

After the wound has been cleaned, the patient should apply a thick layer of an antibiotic cream or ointment, such as the multiingredient antibiotics Neosporin or Polysporin.

Cover the wound

Bandages can help keep the wound clean and keep harmful bacteria out. Have the patient cover blisters that are draining; they’re vulnerable to infection until a scab forms.

Change the dressing

To help prevent infection, tell the patient to apply a new dressing at least once per day or whenever the dressing becomes wet or dirty.

Insert an artificial airway, if necessary, to prevent tongue injury and maintain airway during spasms.
Provide adequate nutrition to meet the patient’s increased metabolic needs. The patient may need nasogastric feedings or total parenteral nutrition. (See Preventing tetanus.)

Botulism

Botulism, a life-threatening paralytic illness, results from an exotoxin produced by the gram-positive, anaerobic bacillus Clostridium botulinum. It occurs with botulism food poisoning, wound botulism, and infant botulism. The mortality from botulism is about 8%; death is usually caused by respiratory failure during the first week of illness.

CAUSES AND INCIDENCE

Botulism is usually the result of ingesting inadequately cooked contaminated foods, especially those with low acid content, such as home-canned fruits and vegetables, sausages, and smoked or preserved fish or meat. Rarely, it’s a result of wound infection with C. botulinum.

Botulism occurs worldwide and affects more adults than children. Recently, findings have shown that an infant’s GI tract can become colonized with C. botulinum from some unknown source, and then the exotoxin is produced within the infant’s intestine. Infant botulism is usually attributed to the ingestion of honey or corn syrup. Incidence had been declining, but the current trend toward home canning has resulted in an upswing (approximately 250 cases per year in the United States) in recent years.

SIGNS AND SYMPTOMS

Symptoms usually appear within 18 to 36 hours (range is 6 hours to 10 days) after the ingestion of contaminated food. Severity varies with the amount of toxin ingested and the patient’s degree of immunocompetence. Generally, early onset (within 24 hours) signals critical and potentially fatal illness. Initial signs and symptoms include dry mouth, sore throat, weakness, dizziness, vomiting, and diarrhea. The cardinal sign of botulism, though, is acute symmetrical cranial nerve impairment (ptosis, diplopia, and dysarthria), followed by descending weakness or paralysis of muscles in the extremities or trunk, and dyspnea from respiratory muscle paralysis. Such impairment doesn’t affect mental or sensory processes and isn’t associated with fever.

Infant botulism usually afflicts infants between ages 3 and 20 weeks and can produce hypotonic (floppy) infant syndrome. Signs and symptoms are constipation, feeble cry, depressed gag reflex, and inability to suck. Cranial nerve deficits also occur in infants and are manifested by a flaccid facial expression, ptosis, and ophthalmoplegia. Infants also develop generalized muscle weakness, hypotonia, and areflexia. Loss of head control may be striking. Respiratory arrest is likely.

DIAGNOSIS

Diagnosis also must rule out other diseases commonly confused with botulism, such as Guillain-Barré syndrome, myasthenia gravis, stroke, staphylococcal food poisoning, tick paralysis, chemical intoxications, carbon monoxide poisoning, fish poisoning, trichinosis, and diphtheria.

TREATMENT

Treatment consists of I.V. or I.M. administration of botulinus antitoxin (available through the Centers for Disease Control and Prevention). Antitoxin is not routinely given for treatment of infant botulism. A new treatment called Baby BIG (botulism immune globulin) is given I.V. and is only available through a special site. If breathing difficulty develops, intubation and mechanical ventilation may be required. I.V. fluids can be given if there are swallowing problems, and a nasogastric tube can also be ordered.

SPECIAL CONSIDERATIONS

If you suspect ingestion of contaminated food:

Obtain a careful history of the patient’s food intake for the past several days. See if other family members exhibit similar symptoms and share a common food history.
Observe carefully for abnormal neurologic signs. Tell the patient’s family to watch for signs of weakness, blurred vision, and slurred speech after he has returned home. If such signs appear, the patient must return to the hospital immediately.
If ingestion has occurred within several hours, induce vomiting, begin gastric lavage, and give a high enema to purge any unabsorbed toxin from the bowel.

If clinical signs of botulism appear:

Admit the patient to the intensive care unit, and monitor cardiac and respiratory functions carefully.
Administer botulinum antitoxin, as ordered, to neutralize any circulating toxin. Before giving the antitoxin, be sure to obtain an accurate patient history of allergies, especially to horses, and perform a skin test. Afterward, watch for anaphylaxis or other hypersensitivity and serum sickness. Keep epinephrine 1:1,000 (for subcutaneous administration) and emergency airway equipment available.
Assess respiratory function every 4 hours. Report decreased vital capacity on inspiratory effort and any signs of respiratory distress.
Closely assess and accurately record neurologic function, including bilateral motor status (reflexes, ability to move arms and legs).
Give I.V. fluids as ordered. Turn the patient often, and encourage deep-breathing exercises. Isolation isn’t required.
As botulism is sometimes fatal, keep the patient and his family informed regarding the course of the disease.
Immediately report all cases of botulism to public health authorities.

Gas gangrene

Gas gangrene results from local infection with the anaerobic, spore-forming, gram-positive rod Clostridium perfringens (or another clostridial species). It occurs in devitalized tissues and results from compromised arterial circulation after trauma, surgery, compound fractures, or lacerations. This rare infection carries a high mortality unless therapy begins immediately; however, with prompt treatment, 80% of patients with gas gangrene of the extremities survive. The prognosis is poorer for gas gangrene in other sites, such as the abdominal wall or the bowel. The usual incubation period is 1 to 4 days but can vary from 3 hours to 6 weeks or longer.

CAUSES AND INCIDENCE

C. perfringens is a normal inhabitant of the GI and female genital tracts; it’s also prevalent in soil. Transmission occurs by entry of organisms during trauma or surgery. Because C. perfringens is anaerobic and spore forming, gas gangrene is usually found in deep wounds, especially those in which tissue necrosis further reduces oxygen supply. Clostridium bacteria produce four different toxins (alpha, beta, epsilon, iota) that can cause potentially fatal symptoms. When C. perfringens invades soft tissues, it produces thrombosis of regional blood vessels, tissue necrosis, localized edema, and damage to the myocardium, liver, and kidneys. Such necrosis releases both carbon dioxide and hydrogen subcutaneously, producing interstitial gas bubbles. Gas gangrene usually occurs in the extremities and in abdominal wounds; it’s less common in the uterus.

Gas gangrene is rare, with only 1,000 to 3,000 cases occurring in the United States annually.

SIGNS AND SYMPTOMS

True gas gangrene produces myositis and another form of this disease, involving only soft tissue, called anaerobic cellulitis. Most signs of infection develop within 72 hours of trauma or surgery. The hallmark of gas gangrene is crepitation (a crackling sensation when the skin is touched), a result of carbon dioxide and hydrogen accumulation as a metabolic by-product in necrotic tissues. Other typical indications are severe localized pain, swelling, and discoloration (usually dusky brown or reddish), with formation of bullae and necrosis within 36 hours from onset of symptoms. The skin over the wound may rupture, revealing dark red or black necrotic muscle, a foul-smelling watery or frothy discharge, intravascular hemolysis, thrombosis of blood vessels, and evidence of infection spread.

In addition to these local symptoms, gas gangrene produces early signs of toxemia and hypovolemia (tachycardia, tachypnea, and hypotension), with moderate fever usually not above 101° F (38.3° C). Although pale, prostrate, and motionless, patients with gas gangrene may exhibit toxic delirium and are extremely apprehensive. Possible sudden death is preceded by delirium and coma and is sometimes accompanied by vomiting, profuse diarrhea, and circulatory collapse.

DIAGNOSIS

Gas gangrene is confirmed by anaerobic cultures of wound drainage showing C. perfringens; a Gram stain of wound drain-age showing large, gram-positive, rod-shaped bacteria; X-rays showing gas in tissues; and blood studies showing leukocytosis and, later, hemolysis.

Diagnosis must rule out synergistic gangrene and necrotizing fasciitis; unlike gas gangrene, both these disorders anesthetize the skin around the wound.

TREATMENT

Treatment includes careful observation for signs of myositis and cellulitis and immediate treatment if these signs appear; immediate wide surgical excision of all affected tissues and necrotic muscle in myositis (delayed or inadequate surgical excision is a fatal mistake); I.V. administration of high-dose penicillin; and, after adequate debridement, hyperbaric oxygenation, if available. For 1 to 3 hours every 6 to 8 hours, the patient is placed in a hyperbaric chamber, exposing him to pressures designed to increase oxygen tension and prevent multiplication of the anaerobic clostridia. Surgery may be performed within the hyperbaric chamber if the chamber is large enough.

SPECIAL CONSIDERATIONS

Careful observation may result in early diagnosis. Look for signs and symptoms of ischemia (cool skin; pallor or cyanosis; sudden, severe pain; sudden edema; and loss of pulses in involved limb).

After the diagnosis:

Throughout this illness, provide adequate fluid replacement, and assess pulmonary and cardiac functions often. Maintain airway and ventilation.
To prevent skin breakdown and further infection, give good skin care. After surgery, provide meticulous wound care. Use contact precautions for significant drainage.
Before penicillin administration, obtain a patient history of allergies; afterward, watch closely for signs of hypersensitivity.
Psychological support is critical, because these patients can remain alert until death, knowing that death is imminent and unavoidable.
Deodorize the room to control foul odor from the wound. Prepare the patient emotionally for a large wound after surgical excision, and refer him for physical rehabilitation, as necessary.
Institute standard precautions. Use contact precautions if drainage is significant. Dispose of drainage material properly, and wear sterile gloves when changing dressings. Spore-forming bacteria aren’t destroyed by ordinary disinfecting methods. Contaminated items should be cleaned and disinfected or sterilized, as appropriate.

Be alert for devitalized tissues, and notify the surgeon promptly.
Position the patient to facilitate drainage, and eliminate all dead spaces in closed wounds.

Actinomycosis

Actinomycosis is a rare infection primarily caused by the gram-positive anaerobic bacillus Actinomyces israelii, which produces granulomatous, suppurative lesions with abscesses. Common infection sites are the head, neck, thorax, and abdomen, but it can spread to contiguous tissues, causing multiple draining sinuses.

CAUSES AND INCIDENCE

A. israelii occurs as part of the normal flora of the throat, tonsillar crypts, and mouth (particularly around carious teeth); infection results from its traumatic introduction into body tissues.

Actinomycosis affects twice as many males— especially those ages 15 to 35—as females. People with dental disease or human immunodeficiency virus infection are at increased risk.

SIGNS AND SYMPTOMS

Symptoms appear from days to months after injury and may vary, depending on the site of infection.

In cervicofacial actinomycosis (lumpy jaw), painful, indurated swellings appear in the mouth or neck up to several weeks after dental extraction or trauma. They gradually enlarge and form fistulas that open onto the skin. Sulfur granules (yellowish gray masses that are actually colonies of A. israelii) appear in the exudate.

In pulmonary actinomycosis, aspiration of bacteria from the mouth into areas of the lungs already anaerobic from infection or atelectasis produces a fever and a cough that becomes productive and occasionally causes hemoptysis. Eventually, empyema follows, a sinus forms through the chest wall, and septicemia may occur.

In GI actinomycosis, ileocecal lesions are caused by swallowed bacteria, which produce abdominal discomfort, fever, sometimes a palpable mass, and an external sinus. This follows intestinal mucosa disruption, usually by surgery or an inflammatory bowel condition such as appendicitis.

Rare sites of actinomycotic infection are the bones, brain, liver, kidneys, and female reproductive organs. Symptoms reflect the organ involved.

SPECIAL CONSIDERATIONS

Dispose of all dressings in a sealed plastic bag.
After surgery, provide proper sterile wound management.
Administer antibiotics as ordered. Before giving the first dose, obtain an accurate patient history of allergies. Watch for hypersensitivity reactions, such as rash, fever, itching, and signs of anaphylaxis. If the patient has a history of any allergies, keep epinephrine 1:1,000 and resuscitation equipment available.

Nocardiosis

Nocardiosis is an acute, subacute, or chronic bacterial infection caused by a weakly grampositive species of the genus Nocardia— usually Nocardia asteroides. It’s most common in men, especially those with a compromised immune system. In patients with brain infection, mortality exceeds 80%; in other forms, mortality is 10% in cases with uncomplicated pneumonia.

CAUSES AND INCIDENCE

Nocardia are aerobic gram-positive bacteria with branching filaments resembling fungi. Normally found in soil, these organisms cause occasional sporadic disease in humans and animals throughout the world. Their incubation period is unknown but is probably several weeks. The usual mode of transmission is inhalation of organisms suspended in dust. Transmission by direct inoculation through puncture wounds or abrasions is less common.

SIGNS AND SYMPTOMS

Nocardiosis originates as a pulmonary infection with a cough that produces thick, tenacious, purulent, mucopurulent, and possibly blood-tinged sputum. It may also cause a fever as high as 105° F (40.6° C), chills, night sweats, anorexia, malaise, and weight loss. This infection may lead to pleurisy, intrapleural effusions, and empyema. Other potential complications include tracheitis, bronchitis, pericarditis, endocarditis, peritonitis, mediastinitis, septic arthritis, and keratoconjunctivitis.

If the infection spreads through the blood to the brain, abscesses form, causing confusion, disorientation, dizziness, headache, nausea, and seizures. Rupture of a brain abscess can cause purulent meningitis. Extrapulmonary, hematogenous spread may cause endocarditis or lesions in the kidneys, liver, subcutaneous tissue, and bone.

DIAGNOSIS

Identifying Nocardia by culture of sputum or discharge is difficult. In many cases, special staining techniques must be used to make the diagnosis, in conjunction with a typical clinical picture (usually progressive pneumonia, despite antibiotic therapy). Occasionally, diagnosis requires biopsy of lung or other tissue. Chest X-rays and computed tomography may show fluffy or interstitial infiltrates, nodules, or abscesses.

In brain infection with meningitis, lumbar puncture shows nonspecific changes such as increased opening pressure. Cerebrospinal fluid shows increased white blood cell and protein levels and decreased glucose levels compared with serum glucose.

SPECIAL CONSIDERATIONS

Because it isn’t transmitted from person to person, nocardiosis requires no isolation.

Provide adequate nourishment through total parenteral nutrition, nasogastric tube feedings, or a balanced diet.
Give the patient tepid sponge baths and antipyretics, as ordered, to reduce his fever.
Monitor for allergic reactions to antibiotics.
High-dose sulfonamide therapy (especially sulfadiazine) predisposes the patient to crystalluria and oliguria; so assess him frequently, force fluids, and alkalinize the urine with sodium bicarbonate, as ordered, to prevent these complications.
In patients with pulmonary infection, administer chest physiotherapy. Auscultate the lungs daily, checking for increased crackles or consolidation. Note and record the amount, color, and thickness of sputum.
In brain infection, regularly assess neurologic function. Watch for signs of increased intracranial pressure, such as a decreased level of consciousness and respiratory abnormalities.
In long-term hospitalization, turn the patient often, and assist with range-of-motion exercises.
Before the patient is discharged, stress the need to follow a regular medication schedule to maintain therapeutic blood levels and to continue drugs even after symptoms subside. Explain the importance of frequent follow-up examinations.
Provide support and encouragement to help the patient and his family cope with this longterm illness.

Clostridium difficile Infection

Clostridium difficile is a gram-positive anaerobic bacterium that typically causes antibioticassociated diarrhea. Symptoms may range from asymptomatic carrier states to severe pseudomembranous colitis and are caused by the exotoxins produced by the organism. Toxin A is an enterotoxin and toxin B is a cytotoxin.

CAUSES AND INCIDENCE

C. difficile colitis can be caused by almost any antibiotic that disrupts the bowel flora, but it’s classically associated with clindamycin use. High-risk groups include individuals on greater numbers of antibiotics, those having abdominal surgery, patients receiving antineoplastics that have an antibiotic activity, immunocompromised individuals, pediatric patients (commonly in day-care centers), and nursing home patients.

Other factors that alter normal intestinal flora include enemas and intestinal stimulants. C. difficile is most often transmitted directly from patient to patient by contaminated hands of facility personnel; it may also be indirectly spread by contaminated equipment such as bedpans, urinals, call bells, rectal thermometers, nasogastric tubes, and contaminated surfaces such as bed rails, floors, and toilet seats.

SIGNS AND SYMPTOMS

Risk of C. difficile begins 1 to 2 days after antibiotic therapy is started and extends for as long as 2 to 3 months after the last dose. The patient may be asymptomatic or may exhibit any of the following symptoms: soft, unformed, or watery diarrhea (more than 3 stools in a 24-hour period) that may be foul smelling or grossly bloody; abdominal pain, cramping, or tenderness; and fever. The patient’s white blood cell count may be elevated to 20,000/µl. In severe cases, toxic megacolon, colonic perforation, and peritonitis may develop.

DIAGNOSIS

Diagnosis is by identification of the toxin through one of these acceptable methods:

cell cytotoxin test—the gold standard for diagnosis of C. difficile; it tests for both toxin A and B; this takes 2 days to perform. It’s highly sensitive and specific for C. difficile.
molecular tests—the Food and Drug Administration has approved polymerase chain reation (PCR) assay test for the gene encoding toxin B.
enzyme immunoassays—slightly less sensitive than the cell cytotoxin test but has a turnaround time of only a few hours. Specificity is excellent.
stool culture—the most sensitive test; has a turnaround time of 2 days to obtain results. Non-toxin-producing strains of C. difficile can be easily identified; discovery of the toxin in stool requires further testing.
endoscopy (flexible sigmoidoscopy)—may be used in a patient who presents with an acute abdomen but no diarrhea, making it difficult to obtain a stool specimen. If pseudomembranes are visualized, treatment for C. difficile is usually initiated.

TREATMENT

After the causative antibiotic is withdrawn (if possible), symptoms resolve in patients who are mildly symptomatic. This is usually the only treatment needed. In more severe cases, metronidazole or vancomycin are effective therapies; metronidazole is the preferred treatment. Retesting for C. difficile is unnecessary if symptoms resolve.

About 10% to 20% of patients experience recurrence with the same organism within 14 to 30 days of treatment. Beyond 30 days, a recurrence may be a relapse or reinfection of C. difficile. If the previous treatment was metronidazole, low-dose vancomycin may be an effective choice.

There’s no evidence to support the effectiveness of eating yogurt or taking lactobacillus. Other experimental treatments involve the administration of yeast Saccharomyces boulardii with metronidazole or vancomycin and biological vaccines to restore the normal GI flora. I.V. immunoglobulin has been used successfully in children and adults with relapsing infections, although it’s still being studied.

SPECIAL CONSIDERATIONS

Patients with known or suspected C. difficile diarrhea who are unable to practice good hygiene should be placed on contact precautions in a single room or in a room with other patients with similar status.
Use contact precautions for contact with blood and body fluids and for all direct contact with the patient and his immediate environment.
Wash your hands with an antiseptic soap after direct contact with the patient or the immediate environment. Alcohol hand rubs will not inactivate C. difficile spores.
A patient who is asymptomatic, without diarrhea or fecal incontinence for 72 hours, and who is able to practice good hygiene may have contact precautions discontinued.

Make sure reusable equipment is disinfected before it’s used on another patient.
Teach good hand-washing technique to prevent the spread of the infection.
Review proper disinfection of contaminated clothing or household items.
Tell the patient to inform health care workers of his condition before admission.

GRAM-NEGATIVE BACILLI

Salmonellosis

A common infection in the United States, salmonellosis is caused by gram-negative bacilli of the genus Salmonella, a member of the Enterobacteriaceae family. It occurs as enterocolitis, bacteremia, localized infection, typhoid, or paratyphoid fever. Nontyphoidal forms usually produce mild to moderate illness with low mortality. (See Types of salmonellosis, page 834.)

Typhoid, the most severe form of salmonellosis, usually lasts from 1 to 4 weeks. Mortality is about 3% in patients who are treated. In those who are untreated, 10% of cases result in fatality, usually as a result of intestinal perforation or hemorrhage, cerebral thrombosis, toxemia, pneumonia, or acute circulatory failure. An attack of typhoid confers lifelong immunity, although the patient may become a carrier. Salmonellosis is 20 times more common in patients with acquired immunodeficiency syndrome. Features are increased incidence of bacteremia, inability to identify the infection source, and tendency of infection to recur after therapy is stopped.

CAUSES AND INCIDENCE

Of an estimated 1,700 serotypes of Salmonella, 10 cause the diseases most common in the United States; all 10 can survive for weeks in water, ice, sewage, or food. Nontyphoidal salmonellosis generally follows the ingestion of contaminated or inadequately processed foods, especially eggs, chicken, turkey, and duck. Proper cooking reduces the risk of contracting salmonellosis. Other causes include contact with infected people or animals or ingestion of contaminated dry milk, chocolate bars, or drugs of animal origin. Salmonellosis may occur in children younger than age 5 from fecal-oral spread. Enterocolitis and bacteremia are common (and more virulent) among infants, elderly persons, and people already weakened by other infections; paratyphoid fever is rare in the United States.

Typhoid usually results from drinking water contaminated by excretions of a carrier or from ingesting contaminated shellfish. (Contamination of shellfish occurs by leakage of sewage from offshore disposal depots.) Most typhoid patients are younger than age 30; most carriers are women older than age 50. Incidence of typhoid in the United States is increasing as a result of travelers returning from endemic areas.

Types of salmonellosis

Type	Cause	Clinical features
Bacteremia	Any Salmonella species, but most commonly S. choleraesuis. Incubation period: variable	Fever, chills, anorexia, weight loss (without GI symptoms), and joint pain
Enterocolitis	Any species of nontyphoidal Salmonella, but usually S. enteritidis. Incubation period: 6 to 48 hours	Mild to severe abdominal pain, diarrhea, sudden fever of up to 102° F (38.9° C), nausea, and vomiting; usually self-limiting, but may progress to enteric fever (resembling typhoid), local abscesses (usually abdominal), dehydration, and septicemia
Localized infections	Usually follows bacteremia caused by Salmonella species	Site of localization determines symptoms; localized abscesses may cause osteomyelitis, endocarditis, bronchopneumonia, pyelonephritis, and arthritis
Paratyphoid	S. paratyphi and S. schottmuelleri (formerly S. paratyphi B). Incubation period: 3 weeks or more	Fever and transient diarrhea; generally resembles typhoid but less severe
Typhoid fever	S. typhi enters the GI tract and invades the bloodstream via the lymphatics, setting up intracellular sites. During this phase, infection of the biliary tract leads to intestinal seeding with millions of bacilli. Involved lymphoid tissues (especially Peyer’s patches in the ilium) enlarge, ulcerate, and necrose, resulting in hemorrhage. Incubation period: usually 1 to 2 weeks	Symptoms of enterocolitis may develop within hours of ingestion of S. typhi; they usually subside before onset of typhoid fever symptoms First week: gradually increasing fever, anorexia, myalgia, malaise, headache, and slow pulse Second week: remittent fever up to 104° F (40° C) usually in the evening, chills, diaphoresis, weakness, delirium, increasing abdominal pain and distention, diarrhea or constipation, cough, moist crackles, tender abdomen with enlarged spleen, and maculopapular rach (especially on abdomen) Third week: persistent fever, increasing fatigue and weakness; usually subsides by end of third week, although relapses may occur Complications: intestinal perforation or hemorrhage, abscesses, thrombophlebitis, cerebral thrombosis, pneumonia, osteomyelitis, myocarditis, acute circulatory failure, and chronic carrier state

SIGNS AND SYMPTOMS

Clinical manifestations of salmonellosis vary but usually include fever, abdominal pain, and severe diarrhea with enterocolitis. Headache, increasing fever, and constipation are more common in typhoidal infection.

PREVENTION Preventing recurrence of salmonellosis

Take the following actions to help your patient prevent a recurrence of salmonellosis:

Explain the causes of salmonella infection.
Show the patient how to wash his hands by wetting them under running water, lathering with soap and scrubbing, rinsing under running water with his fingers pointing down, and drying with a clean towel or paper towel.
Tell the patient to wash his hands after using the bathroom and before eating.
Tell the patient to cook foods thoroughly— especially eggs and chicken—and to refrigerate them at once.
Teach the patient how to avoid crosscontaminating foods by cleaning preparation surfaces with hot, soapy water and drying them thoroughly after use; cleaning surfaces between foods when preparing more than one food; and washing his hands before and after handling each food.
Tell the patient with a positive stool culture to avoid handling food and to use a separate bathroom or clean the bathroom after each use.
Tell the patient to report dehydration, bleeding, or recurrence of signs of salmonella infection.

DIAGNOSIS

Generally, diagnosis depends on isolation of the organism in a culture, particularly blood (in typhoid, paratyphoid, and bacteremia) or feces (in enterocolitis, paratyphoid, and typhoid). Other appropriate culture specimens include urine, bone marrow, pus, and vomitus. In endemic areas, clinical symptoms of enterocolitis allow a working diagnosis before the cultures are positive. The presence of Salmonella typhi in stool 1 or more years after treatment indicates that the patient is a carrier, which is true of 3% of patients.

Widal’s test, an agglutination reaction against somatic and flagellar antigens, may suggest typhoid with a fourfold rise in titer. However, drug use or hepatic disease can also increase these titers and invalidate test results. Other supportive laboratory values may include transient leukocytosis during the 1st week of typhoidal salmonellosis, leukopenia during the 3rd week, and leukocytosis in local infection.

TREATMENT

Antimicrobial therapy for typhoid, paratyphoid, and bacteremia depends on organism sensitivity. It may include amoxicillin, chloramphenicol and, in severely toxemic patients, trimethoprim/sulfamethoxazole, ciprofloxacin, or ceftriaxone. Localized abscesses may also need surgical drainage. Enterocolitis requires a short course of antibiotics only if it causes septicemia or prolonged fever. Other treatments include bed rest and fluid and electrolyte replacement. The administration of camphorated opium tincture, kaolin with pectin, diphenoxylate, codeine, or small doses of morphine may be necessary to relieve diarrhea and control cramps in patients who must remain active.

SPECIAL CONSIDERATIONS

All infections caused by Salmonella must be reported to the state health department.
Follow contact precautions if the patient is incontinent or diapered; otherwise, standard precautions are appropriate. Always wash your hands thoroughly before and after any contact with the patient, and advise other facility personnel to do the same. Teach the patient to use proper hand washing, especially after defecating and before eating or handling food. Wear gloves and a gown when disposing of feces or fecally contaminated objects. Continue precautions until three consecutive stool cultures are negative—the first one taken 48 hours after antibiotic treatment ends, followed by two more at 24-hour intervals.
Observe the patient closely for signs and symptoms of bowel perforation from erosion of intestinal ulcers: sudden pain in the lower right side of the abdomen and abdominal rigidity, possibly after one or more rectal bleeding episodes; sudden fall in temperature or blood pressure; and rising pulse rate (indicating shock).
During acute infection, plan care and activities to allow the patient as much rest as possible. Raise the side rails and use other safety measures, because the patient may become delirious. Assign him a room close to the nurses’ station so he can be checked often. Use a room deodorizer (preferably electric) to minimize odor from diarrhea and to provide a comfortable atmosphere for rest.
Accurately record intake and output. Maintain adequate I.V. hydration. When the patient can tolerate oral feedings, encourage highcalorie fluids such as milkshakes. Watch for constipation.
Provide good skin and mouth care. Turn the patient frequently, and perform mild passive exercises, as indicated. Apply mild heat to the abdomen to relieve cramps.
Don’t administer antipyretics. These mask fever and lead to possible hypothermia. Instead, to promote heat loss through the skin without causing shivering (which keeps fever high by vasoconstriction), apply tepid, wet towels (don’t use alcohol or ice) to the patient’s groin and axillae. To promote heat loss by vasodilation of peripheral blood vessels, use additional wet towels on the arms and legs, wiping with long, vigorous strokes.
After draining the abscesses of a joint, provide heat, elevation, and passive rangeof-motion exercises to decrease swelling and maintain mobility.
If the patient has positive stool cultures on discharge, tell him to be sure to wash his hands after using the bathroom and to avoid preparing uncooked foods, such as salads, for family members. He also shouldn’t work as a food handler until cultures are negative. (See Preventing recurrence of salmonellosis, page 835.)
Report all cases to public health authorities.

Shigellosis

Shigellosis, also known as bacillary dysentery, is an acute intestinal infection caused by the bacteria Shigella, a short, nonmotile, gram-negative rod. Shigella can be classified into four groups, all of which may cause shigellosis: group A (S. dysenteriae), which is most common in Central America and causes particularly severe infection and septicemia; group B (S. flexneri); group C (S. boydii); and group D (S. sonnei). Typically, shigellosis causes a high fever (especially in children), acute self-limiting diarrhea with tenesmus (ineffectual straining at stool) and, possibly, electrolyte imbalance and dehydration. It’s most common in children ages 1 to 4; however, many adults acquire the illness from children.

The prognosis is good. Mild infections usually subside within 10 days; severe infections may persist for 2 to 6 weeks. With prompt treatment, shigellosis is fatal in only 1% of cases, although in severe S. dysenteriae epidemic mortality may reach 8%.

CAUSES AND INCIDENCE

Transmission occurs through the fecal-oral route; by direct contact with contaminated objects; or through ingestion of contaminated food or water. Occasionally, the housefly is a vector.

Shigellosis is endemic in North America, Europe, and the tropics. In the United States, about 18,000 cases appear annually, usually in children or in elderly, debilitated, or malnourished people. Shigellosis commonly occurs among confined populations, such as those in mental institutions or day-care centers.

SIGNS AND SYMPTOMS

After an incubation period of 1 to 7 days (3 days is the average), Shigella organisms invade the intestinal mucosa and cause inflammation. In children, shigellosis usually produces high fever, diarrhea with tenesmus, nausea, vomiting, irritability, drowsiness, and abdominal pain and distention. Within a few days, the child’s stool may contain pus, mucus, and—from the superficial intestinal ulceration typical of this infection—blood. Without treatment, dehydration and weight loss are rapid and overwhelming.

In adults, shigellosis produces sporadic, intense abdominal pain, which may be relieved at first by passing formed stools. Eventually, however, it causes rectal irritability, tenesmus and, in severe infection, headache and prostration. Stools may contain pus, mucus, and blood. Fever may be present.

DIAGNOSIS

Microscopic examination of a fresh stool may reveal mucus, red blood cells, and polymorphonuclear leukocytes; direct immunofluorescence with specific antisera will demonstrate Shigella. Severe infection increases hemagglutinating antibodies. Sigmoidoscopy or proctoscopy may reveal typical superficial ulcerations.

Diagnosis must rule out other causes of diarrhea, such as enteropathogenic Escherichia coli infection, malabsorption diseases, and amebic or viral diseases.

TREATMENT

Treatment of shigellosis includes enteric precautions, low-residue diet and, most important, replacement of fluids and electrolytes with I.V. infusions of normal saline solution (with electrolytes) in sufficient quantities to maintain a urine output of 40 to 50 mL/hour. Antibiotics are of questionable value but may be used in an attempt to eliminate the pathogen and thereby prevent further spread. Ampicillin, tetracycline, or trimethoprim/sulfamethoxazole may be useful in severe cases, especially in children with overwhelming fluid and electrolyte loss. Ciprofloxacin is also used.

Antidiarrheals that slow intestinal motility are contraindicated in shigellosis because they delay fecal excretion of Shigella and prolong fever and diarrhea. An investigational vaccine containing attenuated strains of Shigella appears promising in preventing shigellosis.

SPECIAL CONSIDERATIONS

Supportive care can minimize complications and increase patient comfort.

To prevent dehydration, administer I.V. fluids as ordered. Measure intake and output (including stools) carefully.
Correct identification of Shigella requires examination and culture of fresh stool specimens. Therefore, hand carry specimens directly to the laboratory. Because shigellosis is suspected, include this information on the laboratory slip.
Use a disposable hot-water bottle to relieve abdominal discomfort, and schedule care to conserve patient strength.

During shigellosis outbreaks, obtain stool specimens from all potentially infected staff, and instruct those infected to remain away from work until two stool specimens are negative.
Basic food safety precautions and disinfection of drinking water prevents shigellosis from food and water contamination.
Report cases to the local health authorities.

Escherichia coli and other Enterobacteriaceae infections

The Enterobacteriaceae—a group of mostly aerobic, gram-negative bacilli—cause local and systemic infections, including an invasive diarrhea resembling shigellosis and, more commonly, a noninvasive toxin-mediated diarrhea resembling cholera. With other Enterobacteriaceae, Escherichia coli causes most nosocomial infections. Noninvasive, enterotoxin-producing E. coli infections may be a major cause of diarrheal illness in children in the United States. (See Enterobacterial infections, page 838.)

The prognosis in mild to moderate infection is good. Severe infection requires immediate fluid and electrolyte replacement to avoid fatal dehydration, especially among children, in whom mortality may be quite high.

CAUSES AND INCIDENCE

Although some strains of E. coli exist as part of the normal GI flora, infection usually results from certain nonindigenous strains. For example, noninvasive diarrhea results from two toxins produced by strains called enterotoxic or enteropathogenic E. coli. Enteropathogenic E. coli serotype 0157:H7 is the most well-known strain in the United States. These toxins interact with intestinal juices and promote excessive loss of chloride and water. In the invasive form, E. coli directly invades the intestinal mucosa without producing enterotoxins, thereby causing local irritation, inflammation, and diarrhea. Normal strains can cause infection in immunocompromised patients.

Transmission can occur directly from an infected person or indirectly by ingestion of contaminated food or water or contact with contaminated utensils. Incubation takes 12 to 72 hours.

Incidence of E. coli infection is highest among travelers returning from other countries, particularly Mexico, Southeast Asia, and South America. E. coli infection also induces other diseases, especially in people whose resistance is low. The strain E. coli 0157:H7 has been associated with undercooked hamburger and with animals and petting zoos.

Enterobacterial infections

The Enterobacteriaceae include Escherichia coli, Arizona, Citrobacter, Enterobacter, Erwinia, Hafnia, Klebsiella, Morganella, Proteus, Providencia, Salmonella, Serratia, Shigella, and Yersinia.

Enterobacterial infections are exogenous (from other people or the environment), endogenous (from one part of the body to another), or a combination of both. Enterobacteriaceae infections may cause any of a long list of bacterial diseases: bacterial (gram-negative) pneumonia, empyema, endocarditis, osteomyelitis, septic arthritis, urethritis, cystitis, bacterial prostatitis, urinary tract infection, pyelonephritis, perinephric abscess, abdominal abscesses, cellulitis, skin ulcers, appendicitis, gastroenterocolitis, diverticulitis, eyelid and periorbital cellulitis, corneal conjunctivitis, meningitis, bacteremia, and intracranial abscesses.

Appropriate antibiotic therapy depends on the results of culture and sensitivity tests. Generally, the aminoglycosides, cephalosporins, and penicillins—such as ampicillin and piperacillin—are most effective. Cefepime and quinones are also effective for some infections.

SIGNS AND SYMPTOMS

Effects of noninvasive diarrhea depend on the causative toxin but may include the abrupt onset of watery diarrhea with cramping abdominal pain and, in severe illness, acidosis. Invasive infection produces chills, abdominal cramps, and diarrheal stools containing blood and pus.

Infantile diarrhea from an E. coli infection is usually noninvasive; it begins with loose, watery stools that change from yellow to green and contain little mucus or blood. Vomiting, listlessness, irritability, and anorexia commonly precede diarrhea. This condition can progress to fever, severe dehydration, acidosis, and shock. Bloody diarrhea may occur from infection with E. coli 0157:H7, which has also been associated with hemolytic-uremic syndrome in children.

DIAGNOSIS

Because certain strains of E. coli normally reside in the GI tract, culturing is of little value; a working diagnosis depends on clinical observation. However, if E. coli 0157:H7 is suspected, notify the laboratory so that appropriate testing of stool specimens can be performed.

A firm diagnosis requires sophisticated identification procedures, such as bioassays, that are expensive, time-consuming and, consequently, not widely available. Diagnosis must rule out salmonellosis and shigellosis, other common infections that produce similar signs and symptoms.

SPECIAL CONSIDERATIONS

Keep accurate intake and output records. Measure stool volume and note the presence of blood or pus. Replace fluids and electrolytes as needed, monitoring for decreased serum sodium and chloride levels and signs of gramnegative shock. Watch for signs of dehydration, such as poor skin turgor and dry mouth.
For infants, use contact precautions, give nothing by mouth, administer antibiotics as ordered, and maintain body warmth.

To prevent spread of this infection:

Prevent direct patient contact during epidemics. Report cases to local public health authorities. E. coli 0157:H7 is a reportable disease.
Use proper hand-washing technique. Teach health care personnel, patients, and their families to do the same.
Follow standard precautions. Provide the patient with a private room, wear protective clothing as necessary, such as when handling feces or soiled linens, and perform scrupulous hand washing before entering and after leaving the patient’s room.
Advise travelers to foreign countries to avoid unbottled water and uncooked fruits and vegetables.

Pseudomonas infections

Pseudomonas is a small gram-negative bacillus that produces nosocomial infections, superinfections of various parts of the body, and a rare disease called melioidosis. (See Melioidosis.) This bacillus is also associated with bacteremia, endocarditis, and osteomyelitis in drug addicts. In local Pseudomonas infections, treatment is usually successful and complications rare; however, in patients with any type of lowered immunologic resistance—premature neonates; elderly patients; patients with debilitating disease, burns, or wounds; or patients receiving chemotherapy or radiation therapy— septicemic Pseudomonas infections are serious and commonly fatal.

CAUSES AND INCIDENCE

The most common species of Pseudomonas is P. aeruginosa. Other species that typically cause disease in humans include Xanthomonas maltophilia (formerly known as P. maltophilia), Burkholderia cepacia (formerly known as P. cepacia), P. fluorescens, P. testosteroni, P. acidovorans, P. alcaligenes, P. stutzeri, P. putrefaciens, and P. putida. These organisms are commonly found in liquids that have been allowed to stand for a long time, such as benzalkonium chloride, saline solution, penicillin, water in flower vases, and fluids in incubators, humidifiers, and inhalation therapy equipment. P. aeruginosa is associated with chronic obstructive pulmonary disease. B. cepacia is the organism most closely associated with cystic fibrosis, although P. aeruginosa is also associated with it. In elderly patients, Pseudomonas infection usually enters through the genitourinary tract; in neonates and infants, through the umbilical cord, skin, and GI tract.

SIGNS AND SYMPTOMS

The most common infections associated with Pseudomonas include skin infections (such as burns and pressure ulcers), urinary tract infections, infant epidemic diarrhea and other diarrheal illnesses, bronchitis, pneumonia, bronchiectasis, meningitis, corneal ulcers, mastoiditis, otitis externa, otitis media, endocarditis, and bacteremia.

Drainage in Pseudomonas infections has a distinct, sickly sweet odor and a greenishblue pus that forms a crust on wounds. Other symptoms depend on the site of infection. For example, when it invades the lungs, Pseudomonas causes pneumonia with fever, chills, and a productive cough.

Melioidosis

Melioidosis, also called Whitmore’s disease; results from wound penetration, inhalation, or ingestion of the gram-negative bacteria produced by the Burkholderia species (gram-negative rods). Although it was once confined to Southeast Asia, Central America, South America, Madagascar, and Guam, incidence in the United States has risen as a result of the influx of Southeast Asians. It is also an organism that is a potential agent for biological warfare and terrorism.

Melioidosis occurs in two forms: chronic melioidosis, which causes osteomyelitis and lung abscesses, and the rare acute melioidosis, which causes pneumonia, bacteremia, and prostration. Acute melioidosis is commonly fatal; however, most melioidosis infections are chronic and asymptomatic, producing clinical symptoms only with accompanying malnutrition, major surgery, or severe burns.

Diagnostic measures consist of isolation of P. pseudomallei in a culture of exudate, blood, or sputum; serology tests (complement fixation, passive hemagglutination); and chest X-ray (findings resemble tuberculosis). Treatment includes oral tetracycline and trimethoprim/sulfamethoxazole, abscess drainage and, in severe cases, chloramphenicol until X-rays show resolution of primary abscesses.

The prognosis is good because most patients have a mild infection and acquire permanent immunity; aggressive use of antibiotics and sulfonamides has improved the prognosis in acute melioidosis.

TREATMENT

In the debilitated or otherwise vulnerable patient with clinical evidence of Pseudomonas infection, treatment should begin immediately, without waiting for results of laboratory tests. Antibiotic treatment includes aminoglycosides, such as gentamicin or tobramycin, combined with an antipseudomonal penicillin, such as ticarcillin or piperacillin. An alternative combination is amikacin and a similar penicillin or imipenem and cilastatin. Such combination therapy is necessary because Pseudomonas quickly becomes resistant to ticarcillin alone.

Local Pseudomonas infections or septicemia secondary to wound infection requires 1% acetic acid irrigations; topical applications of colistimethate, polymyxin B, and silver sulfadiazine cream; and debridement or drainage of the infected wound.

SPECIAL CONSIDERATIONS

Observe and record the character of wound exudate and sputum.
Before administering antibiotics, ask the patient about a history of drug allergies, especially to penicillin. If combinations of piperacillin or ticarcillin and an aminoglycoside are ordered, schedule the doses 1 hour apart (ticarcillin may decrease the antibiotic effect of the aminoglycoside). Don’t give both antibiotics through the same administration set.
Monitor the patient’s renal function (output, blood urea nitrogen level, specific gravity, urinalysis, and creatinine level) during treatment with aminoglycosides. Obtain drug levels to ensure effectiveness.
Protect immunocompromised patients from exposure to this infection. Proper hand washing and sterile techniques prevent further spread. (See Preventing Pseudomonas infection.)

Cholera

Cholera (also known as Asiatic cholera or epidemic cholera) is an acute enterotoxin-mediated GI infection caused by the gram-negative bacillus Vibrio cholerae. It produces profuse diarrhea, vomiting, massive fluid and electrolyte loss and, possibly, hypovolemic shock, metabolic acidosis, and death. A similar bacterium, Vibrio parahaemolyticus, causes food poisoning. (See Vibrio Parahaemolyticus food Poisoning.)

Even with prompt diagnosis and treatment, cholera is fatal in up to 2% of children; in adults, it’s fatal in less than 1%. However, untreated cholera may be fatal in as many as 50% of patients. Cholera infection confers only transient immunity.

CAUSES AND INCIDENCE

Humans are the only hosts and victims of V. cholerae, a motile, aerobic organism. It’s transmitted through food and water contaminated with fecal material from carriers or people with active infections. Cholera is most common in Africa, southern and Southeast Asia, and the Middle East, although outbreaks have occurred in Japan, Australia, and Europe. The incidence of cholera in the United States is rare. However, U.S. travelers to areas with epidemic cholera may be exposed to the bacterium.

Cholera occurs during the warmer months and is most prevalent among lower socioeconomic groups. In India, it’s common among children ages 1 to 5, but in other endemic areas, it’s equally distributed among all age-groups. Susceptibility to cholera may be increased by a deficiency or an absence of hydrochloric acid.

SIGNS AND SYMPTOMS

After an incubation period ranging from several hours to 5 days, cholera produces acute, painless, profuse, watery diarrhea and effortless vomiting (without preceding nausea). As diarrhea worsens, the stools contain white flecks of mucus (rice-water stools). Because of massive fluid and electrolyte losses from diarrhea and vomiting (fluid loss in adults may reach 1 L/hour), cholera causes intense thirst, weakness, loss of skin turgor, wrinkled skin, sunken eyes, pinched facial expression, muscle cramps (especially in the extremities), cyanosis, oliguria, tachycardia, tachypnea, thready or absent peripheral pulses, falling blood pressure, fever, and inaudible, hypoactive bowel sounds.

Patients usually remain oriented but apathetic, although small children may become stuporous or develop seizures. If complications don’t occur, the symptoms subside and the patient recovers within a week. However, if treatment is delayed or inadequate, cholera may lead to metabolic acidosis, uremia and, possibly, coma and death. About 3% of patients who recover continue to carry V. cholerae in the gallbladder; however, most patients are free from the infection after about 2 weeks.

DIAGNOSIS

In endemic areas or during epidemics, characteristic clinical features strongly suggest cholera.

A dark-field microscopic examination of fresh feces showing rapidly moving bacilli (like shooting stars) allows for a quick, tentative diagnosis. Immunofluorescence also allows rapid diagnosis. Diagnosis must rule out Escherichia coli infection, salmonellosis, and shigellosis.

TREATMENT

Improved sanitation and the administration of cholera vaccine to travelers in endemic areas can control this disease. Unfortunately, the vaccine now available confers only 60% to 80% immunity and is effective for only 3 to 6 months. Consequently, vaccination is impractical for residents of endemic areas.

Treatment requires rapid I.V. infusion of large amounts (50 to 100 ml/minute) of isotonic saline solution, alternating with isotonic sodium bicarbonate or sodium lactate. Potassium replacement may be added to the I.V. solution. Antibiotic therapy using such drugs as tetracycline, trimethoprim/sulfamethoxazole, doxycycline, erythromycin, and ciprofloxacin can shorten the course of infection and reduce the rehydration requirement.

Vibrio parahaemolyticus food poisoning

Vibrio parahaemolyticus is a common cause of gastroenteritis in Japan. Outbreaks also occur on American cruise ships and in the eastern and southeastern coastal areas of the United States, especially during the summer.

V. parahaemolyticus, which thrives in a salty environment, is transmitted by ingesting uncooked or undercooked contaminated shellfish, particularly crab, oysters, and shrimp. After an incubation period of 2 to 48 hours, V. parahaemolyticus causes watery diarrhea, moderately severe cramps, nausea, vomiting, headache, weakness, chills, and fever. Food poisoning is usually selflimiting and subsides spontaneously within 2 days. Occasionally, however, it’s more severe, and may even be fatal in debilitated or elderly persons.

Diagnosis requires bacteriologic examination of vomitus, blood, stool smears, or fecal specimens collected by rectal swab. Diagnosis must rule out not only other causes of food poisoning, but also other acute GI disorders.

Treatment is supportive, consisting primarily of bed rest and oral fluid replacement. I.V. replacement therapy is seldom necessary, but oral tetracycline may be prescribed. Thorough cooking of seafood prevents this infection.

When I.V. infusions have corrected hypovolemia, fluid infusion decreases to quantities sufficient to maintain normal pulse and skin turgor or to replace fluid loss through diarrhea. An oral glucose-electrolyte solution can substitute for I.V. infusions. In mild cholera, oral fluid replacement is adequate. If symptoms persist despite fluid and electrolyte replacement, treatment includes tetracycline.

SPECIAL CONSIDERATIONS

A cholera patient requires contact precautions, supportive care, and close observation during the acute phase.

Wear gloves when handling fecescontaminated articles and wash your hands after leaving the patient’s room.
Use contact precautions for diapered or incontinent persons for the duration of illness or to control institutional outbreaks.
Monitor output (including stool volume) and I.V. infusion accurately. To detect overhydration, carefully observe neck veins, take serial patient weights, and auscultate the lungs (fluid loss in cholera is massive, and improper replacement may cause potentially fatal renal insufficiency).
Protect the patient’s family by administering oral tetracycline or doxycycline, if ordered.
Advise anyone traveling to an endemic area to boil all drinking water and avoid uncooked vegetables and unpeeled fruits.
Report all cases to public health authorities.

Septic shock

Second only to cardiogenic shock as the leading cause of shock-related death, septic shock causes inadequate tissue perfusion, abnormalities of oxygen supply and demand, metabolic changes, and circulatory collapse. It typically occurs among hospitalized patients, usually as a result of bacterial infection. About 25% of patients who develop gram-negative bacteremia go into shock. Unless vigorous treatment begins promptly, preferably before symptoms fully develop, septic shock rapidly progresses to death (in many cases within a few hours) in up to 80% of these patients. Septic shock is the most common cause of death in acute care units in the United States.

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