Infection



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).


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.


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:








  • 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.





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.


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.





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.





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.





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.





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.





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.






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.





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.





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.





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.






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.





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.





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.





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.




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.







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.





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.





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.





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.






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.





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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Aug 27, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Infection

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