Bacterial Infections of the Circulatory and Lymphatic Systems Quiz

PDF page 1124: mucosa. Breaches may occur through fairly common occurrences, such as insect bites or small wounds. Even the act of tooth brushing, which can cause small ruptures in the gums, may introduce bacteria into the circulatory system. In most cases, the bacteremia that results from such common exposures is transient and remains below the threshold of detection. In severe cases, bacteremia can lead to septicemia with dangerous complications such as toxemia, sepsis, and septic shock. In these situations, it is often the immune response to the infection that results in the clinical signs and symptoms rather than the microbes themselves.

PDF page 1124: Bacteria are the most common pathogens associated with the development of sepsis, and septic shock. The most common infection associated with sepsis is bacterial pneumonia (see Bacterial Infections of the Respiratory Tract), accounting for about half of all cases, followed by intra-abdominal infections (Bacterial Infections of

PDF page 1124: Toxic Shock Syndrome and Streptococcal Toxic Shock-Like Syndrome Toxemia associated with infections caused by Staphylococcus aureus can cause staphylococcal toxic shock syndrome (TSS). Some strains of S. aureus produce a superantigen called toxic shock syndrome toxin-1 (TSST-1). TSS may occur as a complication of other localized or systemic infections such as pneumonia, osteomyelitis, sinusitis, and skin wounds (surgical, traumatic, or burns). Those at highest risk for staphylococcal TSS are women with preexisting S. aureus colonization of the vagina who leave tampons, contraceptive sponges, diaphragms, or other devices in the vagina for longer than the recommended time. Staphylococcal TSS is characterized by sudden onset of vomiting, diarrhea, myalgia, body temperature higher than 38.9 °C (102.0 °F), and rapid-onset hypotension with a systolic blood pressure less than 90 mm Hg for adults; a diffuse erythematous rash that leads to peeling and shedding skin 1 to 2 weeks after onset; and additional involvement

PDF page 1125: than staphylococcal TSS, with about 50% of patients developing S. pyogenes bacteremia and necrotizing fasciitis. In contrast to staphylococcal TSS, STSS is more likely to cause acute respiratory distress syndrome (ARDS), a rapidly progressive disease characterized by fluid accumulation in the lungs that inhibits breathing and causes hypoxemia (low oxygen levels in the blood). STSS is associated with a higher mortality rate (20%–60%), even with aggressive therapy. STSS usually develops in patients with a streptococcal soft-tissue infection such as bacterial cellulitis, necrotizing fasciitis, pyomyositis (pus formation in muscle caused by infection), a recent influenza A infection, or chickenpox.

PDF page 1125: A type of sepsis called puerperal sepsis, also known as puerperal infection, puerperal fever, or childbed fever, is a nosocomial infection associated with the period of puerperium—the time following childbirth during which the mother’s reproductive system returns to a nonpregnant state. Such infections may originate in the genital tract, breast, urinary tract, or a surgical wound. Initially the infection may be limited to the uterus or other local site of infection, but it can quickly spread, resulting in peritonitis, septicemia, and death. Before the 19th century work of Ignaz Semmelweis and the widespread acceptance of germ theory (see Modern Foundations of Cell Theory), puerperal sepsis was a major cause of mortality among new mothers in the first few days following childbirth. Puerperal sepsis is often associated with Streptococcus pyogenes, but numerous other bacteria can also be responsible. Examples include gram-positive bacterial (e.g. Streptococcus spp., Staphylococcus spp., and Enterococcus spp.), gram-negative bacteria (e.g. Chlamydia spp., Escherichia coli, Klebsiella spp., and Proteus spp.), as well as anaerobes such as Peptostreptococcus spp., Bacteroides spp., and Clostridium spp. In cases caused by S. pyogenes, the bacteria attach to host tissues using M protein and produce a carbohydrate capsule to avoid phagocytosis. S. pyogenes also

PDF page 1126: Also called septic arthritis, infectious arthritis can be either an acute or a chronic condition. Infectious arthritis is characterized by inflammation of joint tissues and is most often caused by bacterial pathogens. Most cases of acute infectious arthritis are secondary to bacteremia, with a rapid onset of moderate to severe joint pain and swelling that limits the motion of the affected joint. In adults and young children, the infective pathogen is most often introduced directly through injury, such as a wound or a surgical site, and brought to the joint through the circulatory system. Acute infections may also occur after joint replacement surgery. Acute infectious arthritis often occurs in patients with an immune system impaired by other viral and bacterial infections. S. aureus is the most common cause of acute septic arthritis in the general population of adults and young children. Neisseria gonorrhoeae is an important cause of acute infectious arthritis in sexually active individuals. Chronic infectious arthritis is responsible for 5% of all infectious arthritis cases and is more likely to occur in patients with other illnesses or conditions. Patients at risk include those who have an HIV infection, a bacterial or fungal infection, prosthetic joints, rheumatoid arthritis (RA), or who are undergoing immunosuppressive chemotherapy. Onset is often in a single joint; there may be little or no pain, aching pain that may be mild, gradual swelling, mild warmth, and minimal or no redness of the joint area. Diagnosis of infectious arthritis requires the aspiration of a small quantity of synovial fluid from the afflicted joint. Direct microscopic evaluation, culture, antimicrobial susceptibility testing, and polymerase chain reaction (PCR) analyses of the synovial fluid are used to identify the potential pathogen. Typical treatment includes administration of appropriate antimicrobial drugs based on antimicrobial susceptibility testing. For nondrug-resistant bacterial strains, β-lactams such as oxacillin and cefazolin are often prescribed for staphylococcal infections. Third-generation cephalosporins (e.g., ceftriaxone) are used for increasingly prevalent β-lactam-resistant Neisseria infections. Infections by Mycobacterium spp. or fungi are treated with appropriate long-term antimicrobial therapy. Even with treatment, the prognosis is often poor for those infected. About 40% of patients with nongonnococcal infectious

PDF page 1126: Osteomyelitis is an inflammation of bone tissues most commonly caused by infection. These infections can either be acute or chronic and can involve a variety of different bacteria. The most common causative agent of osteomyelitis is

PDF page 1126: S. aureus. However, M. tuberculosis, Pseudomonas aeruginosa, Streptococcus pyogenes, S. agalactiae, species in the

PDF page 1126: Enterobacteriaceae, and other microorganisms can also cause osteomyelitis, depending on which bones are involved. In adults, bacteria usually gain direct access to the bone tissues through trauma or a surgical procedure involving prosthetic joints. In children, the bacteria are often introduced from the bloodstream, possibly spreading from focal infections. The long bones, such as the femur, are more commonly affected in children because of the more extensive

PDF page 1127: Infections with S. pyogenes have a variety of manifestations and complications generally called sequelae. As mentioned, the bacterium can cause suppurative infections like puerperal fever. However, this microbe can also cause nonsuppurative sequelae in the form of acute rheumatic fever (ARF), which can lead to rheumatic heart disease, thus impacting the circulatory system. Rheumatic fever occurs primarily in children a minimum of 2–3 weeks after an episode of untreated or inadequately treated pharyngitis (see Bacterial Infections of the Respiratory Tract). At one time, rheumatic fever was a major killer of children in the US; today, however, it is rare in the US because of early diagnosis and treatment of streptococcal pharyngitis with antibiotics. In parts of the world where diagnosis and treatment are not readily available, acute rheumatic fever and rheumatic heart disease are still major causes of

PDF page 1127: mortality in children. Rheumatic fever is characterized by a variety of diagnostic signs and symptoms caused by nonsuppurative, immunemediated damage resulting from a cross-reaction between patient antibodies to bacterial surface proteins and similar proteins found on cardiac, neuronal, and synovial tissues. Damage to the nervous tissue or joints, which leads to joint pain and swelling, is reversible. However, damage to heart valves can be irreversible and is worsened by repeated episodes of acute rheumatic fever, particularly during the first 3–5 years after the first rheumatic fever attack. The inflammation of the heart valves caused by cross-reacting antibodies leads to scarring and stiffness of the valve leaflets. This, in turn, produces a characteristic heart murmur. Patients who have previously developed rheumatic fever and who subsequently develop recurrent pharyngitis due to S. pyogenes are at high risk for a recurrent attacks of rheumatic fever.

PDF page 1128: The endocardium is a tissue layer that lines the muscles and valves of the heart. This tissue can become infected by a variety of bacteria, including gram-positive cocci such as Staphylococcus aureus, viridans streptococci, and Enterococcus faecalis, and the gram-negative so-called HACEK bacilli: Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae. The resulting inflammation is called endocarditis, which can be described as either acute or subacute. Causative agents typically enter the bloodstream during accidental or intentional breaches in the normal barrier defenses (e.g., dental procedures, body piercings, catheterization, wounds). Individuals with preexisting heart damage, prosthetic valves and other cardiac devices, and those with a history of rheumatic fever have a higher risk for endocarditis. This disease can rapidly destroy the heart valves and, if untreated, lead to death in just a few days. In subacute bacterial endocarditis, heart valve damage occurs slowly over a period of months. During this time, blood clots form in the heart, and these protect the bacteria from phagocytes. These patches of tissue-associated bacteria are called vegetations. The resulting damage to the heart, in part resulting from the immune response causing fibrosis of heart valves, can necessitate heart valve replacement (Figure 25.6). Outward signs of subacute endocarditis may include a fever. Diagnosis of infective endocarditis is determined using the combination of blood cultures, echocardiogram, and clinical symptoms. In both acute and subacute endocarditis, treatment typically involves relatively high doses of intravenous antibiotics as determined by antimicrobial susceptibility testing. Acute endocarditis is often treated with a combination of ampicillin, nafcillin, and gentamicin for synergistic coverage of Staphylococcus spp. and Streptococcus spp. Prosthetic-valve endocarditis is often treated with a combination of vancomycin, rifampin, and gentamicin. Rifampin is necessary to treat individuals with infection of prosthetic valves or other foreign bodies because rifampin can penetrate the biofilm of most of the pathogens that infect these devices. Staphylcoccus spp. and Streptococcus spp. can also infect and cause inflammation in the tissues surrounding the heart, a condition called acute pericarditis. Pericarditis is marked by chest pain, difficulty breathing, and a dry cough. In most cases, pericarditis is self-limiting and clinical intervention is not necessary. Diagnosis is made with the aid of a chest radiograph, electrocardiogram, echocardiogram, aspirate of pericardial fluid, or biopsy of pericardium. Antibacterial medications may be prescribed for infections associated with pericarditis; however, pericarditis can also be caused other pathogens, including viruses (e.g., echovirus, influenza virus), fungi (e.g., Histoplasma spp., Coccidioides spp.), and eukaryotic parasites (e.g., Toxoplasma spp.).

PDF page 1128: The endocardium is a tissue layer that lines the muscles and valves of the heart. This tissue can become infected by a variety of bacteria, including gram-positive cocci such as Staphylococcus aureus, viridans streptococci, and Enterococcus faecalis, and the gram-negative so-called HACEK bacilli: Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae. The resulting inflammation is called endocarditis, which can be described as either acute or subacute. Causative agents typically enter the bloodstream during accidental or intentional breaches in the normal barrier defenses (e.g., dental procedures, body piercings, catheterization, wounds). Individuals with preexisting heart damage, prosthetic valves and other cardiac devices, and those with a history of rheumatic fever have a higher risk for endocarditis. This disease can rapidly destroy the heart valves and, if untreated, lead to death in just a few days. In subacute bacterial endocarditis, heart valve damage occurs slowly over a period of months. During this time, blood clots form in the heart, and these protect the bacteria from phagocytes. These patches of tissue-associated bacteria are called vegetations. The resulting damage to the heart, in part resulting from the immune response causing fibrosis of heart valves, can necessitate heart valve replacement (Figure 25.6). Outward signs of subacute endocarditis may include a fever. Diagnosis of infective endocarditis is determined using the combination of blood cultures, echocardiogram, and clinical symptoms. In both acute and subacute endocarditis, treatment typically involves relatively high doses of intravenous antibiotics as determined by antimicrobial susceptibility testing. Acute endocarditis is often treated with a combination of ampicillin, nafcillin, and gentamicin for synergistic coverage of Staphylococcus spp. and Streptococcus spp. Prosthetic-valve endocarditis is often treated with a combination of vancomycin, rifampin, and gentamicin. Rifampin is necessary to treat individuals with infection of prosthetic valves or other foreign bodies because rifampin can penetrate the biofilm of most of the pathogens that infect these devices. Staphylcoccus spp. and Streptococcus spp. can also infect and cause inflammation in the tissues surrounding the heart, a condition called acute pericarditis. Pericarditis is marked by chest pain, difficulty breathing, and a dry cough. In most cases, pericarditis is self-limiting and clinical intervention is not necessary. Diagnosis is made with the aid of a chest radiograph, electrocardiogram, echocardiogram, aspirate of pericardial fluid, or biopsy of pericardium. Antibacterial medications may be prescribed for infections associated with pericarditis; however, pericarditis can also be caused other pathogens, including viruses (e.g., echovirus, influenza virus), fungi (e.g., Histoplasma spp., Coccidioides spp.), and eukaryotic parasites (e.g., Toxoplasma spp.).