Streptococci of medical importance are listed in Table 15–3. All but one of these streptococci are discussed in this section; S. pneumoniae is discussed separately at the end of this chapter because it is so important.
Table 15–3Streptococci of Medical Importance ||Download (.pdf) Table 15–3 Streptococci of Medical Importance
|Species ||Lancefield Group ||Typical Hemolysis ||Diagnostic Features1 |
|S. pyogenes ||A ||β ||Bacitracin-sensitive |
|S. agalactiae ||B ||β ||Bacitracin-resistant; hippurate hydrolyzed |
|E. faecalis ||D ||α or β or none ||Growth in 6.5% NaCl2 |
|S. bovis3 ||D ||α or none ||No growth in 6.5% NaCl |
|S. pneumoniae ||NA4 ||α ||Bile-soluble; inhibited by optochin |
|Viridans group5 ||NA ||α ||Not bile-soluble; not inhibited by optochin |
Streptococci cause a wide variety of infections. S. pyogenes (group A Streptococcus) is the leading bacterial cause of pharyngitis (Figure 15–9) and cellulitis (Figure 15–10). It is an important cause of impetigo (see Figure 15–4), erysipelas, necrotizing fasciitis, scarlet fever, and streptococcal toxic shock syndrome. It is also the inciting factor of two important immunologic diseases, namely, rheumatic fever and acute glomerulonephritis. Streptococcus agalactiae (group B Streptococcus) is the leading cause of neonatal sepsis and meningitis. Enterococcus faecalis is an important cause of hospital-acquired urinary tract infections and endocarditis. Viridans group streptococci are the most common cause of endocarditis (Figure 15–11). Streptococcus bovis (also known as Streptococcus gallolyticus) is an uncommon cause of endocarditis.
Pharyngitis. Note erythema of soft palate, uvula, and posterior pharynx and swelling of the uvula. The most common bacterial cause of pharyngitis is Streptococcus pyogenes. Note: The curved white lines on the uvula and the palate are artifacts of photography. (Reproduced with permission from Centers for Disease Control and Prevention. CDC #6323.)
Cellulitis. Note erythema and swelling of the dorsum of the foot. Streptococcus pyogenes is the most common cause of cellulitis. (Reproduced with permission from Usatine RP, Smith MA, Mayeaux EJ Jr, et al. The Color Atlas of Family Medicine. New York, NY: McGraw-Hill Education; 2009. Photo contributor: Richard P. Usatine, MD.)
Endocarditis. Note vegetations (black arrows) on mitral valve. Viridans streptococci are the most common cause of subacute bacterial endocarditis. (Reproduced with permission from Longo DL, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine, 18th ed. New York, NY: McGraw-Hill Education; 2012.)
Streptococci are spherical gram-positive cocci arranged in chains or pairs (Figure 15–12). All streptococci are catalase-negative, whereas staphylococci are catalase-positive (see Table 15–3).
Streptococcus pyogenes—Gram stain. Arrow points to a long chain of gram-positive cocci. (Used with permission from Professor Shirley Lowe, University of California, San Francisco School of Medicine.)
One of the most important characteristics for identification of streptococci is the type of hemolysis (Figure 15–13).
α-Hemolysis and β-hemolysis on blood agar—Short arrow points to an α-hemolytic colony, probably a viridans group Streptococcus. Long arrow points to a β-hemolytic colony, probably Streptococcus pyogenes. The specimen was a throat swab taken from a person with a sore throat. (Used with permission from Professor Shirley Lowe, University of California, San Francisco School of Medicine.)
α-Hemolytic streptococci form a green zone around their colonies as a result of incomplete lysis of red blood cells in the agar. The green color is formed when hydrogen peroxide produced by the bacteria oxidizes hemoglobin (red color) to biliverdin (green color).
β-Hemolytic streptococci form a clear zone around their colonies because complete lysis of the red cells occurs. β-Hemolysis is due to the production of enzymes (hemolysins) called streptolysin O and streptolysin S (see “Pathogenesis” later).
Some streptococci are nonhemolytic (γ-hemolysis).
There are two important antigens of β-hemolytic streptococci:
C carbohydrate determines the group of β-hemolytic streptococci. It is located in the cell wall, and its specificity is determined by an amino sugar. For example, group A β-hemolytic streptococci (S. pyogenes) are distinguished from group B β-hemolytic streptococci (S. agalactiae) because they have a different C carbohydrate.
M protein is the most important virulence factor of S. pyogenes. It protrudes from the outer surface of the cell and blocks phagocytosis (i.e., it is antiphagocytic). It inactivates C3b, a component of complement that opsonizes the bacteria prior to phagocytosis (see Chapter 63). Strains of S. pyogenes that do not produce M protein are nonpathogenic.
M protein also determines the type of group A β-hemolytic streptococci. There are approximately 100 serotypes based on the M protein, which explains why multiple infections with S. pyogenes can occur. Antibody to M protein provides type-specific immunity.
Strains of S. pyogenes that produce certain M protein types are rheumatogenic (i.e., cause primarily rheumatic fever), whereas strains of S. pyogenes that produce other M protein types are nephritogenic (i.e., cause primarily acute glomerulonephritis). Although M protein is the main antiphagocytic component of S. pyogenes, the organism also has a polysaccharide capsule that plays a role in retarding phagocytosis.
Classification of Streptococci
These are arranged into groups A–U (known as Lancefield groups) on the basis of antigenic differences in C carbohydrate. In the clinical laboratory, the group is determined by precipitin tests with specific antisera or by immunofluorescence.
Group A streptococci (S. pyogenes) are one of the most important human pathogens. They are the most frequent bacterial cause of pharyngitis and a very common cause of skin infections. They adhere to pharyngeal epithelium via pili composed of lipoteichoic acid and M protein. Many strains have a hyaluronic acid capsule that is antiphagocytic. The growth of S. pyogenes on agar plates in the laboratory is inhibited by the antibiotic bacitracin, an important diagnostic criterion (Figure 15–14).
Bacitracin test—Arrow points to zone of inhibition of growth of group A streptococci (Streptococcus pyogenes) caused by bacitracin that has diffused from the disk labeled A. Upper half of blood agar plate shows β-hemolysis caused by group A streptococci, except in the region around the bacitracin disk. Lower half of blood agar plate shows β-hemolysis caused by group B streptococci (Streptococcus agalactiae), and there is no zone of inhibition around the bacitracin disk. (Used with permission from Professor Shirley Lowe, University of California, San Francisco School of Medicine.)
Group B streptococci (S. agalactiae) colonize the genital tract of some women and can cause neonatal meningitis and sepsis. They are usually bacitracin-resistant. They hydrolyze (break down) hippurate, an important diagnostic criterion.
Group D streptococci include enterococci (e.g., E. faecalis and Enterococcus faecium) and nonenterococci (e.g., S. bovis). Enterococci are members of the normal flora of the colon and are noted for their ability to cause urinary, biliary, and cardiovascular infections. They are very hardy organisms; they can grow in hypertonic (6.5%) saline or in bile and are not killed by penicillin G. As a result, a synergistic combination of penicillin and an aminoglycoside (e.g., gentamicin) is required to kill enterococci. Vancomycin can also be used, but vancomycin-resistant enterococci (VRE) have emerged and become an important and much feared cause of life-threatening nosocomial infections. More strains of E. faecium are vancomycin-resistant than are strains of E. faecalis.
Nonenterococcal group D streptococci, such as S. bovis, can cause similar infections but are much less hardy organisms (e.g., they are inhibited by 6.5% NaCl and killed by penicillin G). Note that the hemolytic reaction of group D streptococci is variable: most are α-hemolytic, but some are β-hemolytic, and others are nonhemolytic.
Groups C, E, F, G, H, and K–U streptococci infrequently cause human disease.
Some streptococci produce no hemolysis; others produce α-hemolysis. The principal α-hemolytic organisms are S. pneumoniae (pneumococci) and the viridans group of streptococci (e.g., Streptococcus mitis, Streptococcus sanguinis, and Streptococcus mutans). Pneumococci and viridans streptococci are distinguished in the clinical laboratory by two main criteria: (1) the growth of pneumococci is inhibited by optochin, whereas the growth of viridans streptococci is not inhibited; and (2) colonies of pneumococci dissolve when exposed to bile (bile-soluble), whereas colonies of viridans streptococci do not dissolve.
Viridans streptococci are part of the normal flora of the human pharynx and intermittently reach the bloodstream to cause infective endocarditis. S. mutans synthesizes polysaccharides (dextrans) that are found in dental plaque and lead to dental caries. Streptococcus intermedius and Streptococcus anginosus (also known as the S. anginosus-milleri group) are usually α-hemolytic or nonhemolytic, but some isolates are β-hemolytic. They are found primarily in the mouth and colon.
These grow under anaerobic or microaerophilic conditions and produce variable hemolysis. Peptostreptococci are members of the normal flora of the gut, mouth, and female genital tract and participate in mixed anaerobic infections. The term mixed anaerobic infections refers to the fact that these infections are caused by multiple bacteria, some of which are anaerobes and others are facultatives. For example, peptostreptococci and viridans streptococci, both members of the oral flora, are often found in brain abscesses following dental surgery. Peptostreptococcus magnus and Peptostreptococcus anaerobius are the species frequently isolated from clinical specimens.
Most streptococci are part of the normal flora of the human throat, skin, and intestines but produce disease when they gain access to tissues or blood. Viridans streptococci and S. pneumoniae are found chiefly in the oropharynx; S. pyogenes is found on the skin and in the oropharynx in small numbers; S. agalactiae occurs in the vagina and colon; and both the enterococci and anaerobic streptococci are located in the colon.
Group A streptococci (S. pyogenes) cause disease by three mechanisms: (1) pyogenic inflammation, which is induced locally at the site of the organisms in tissue; (2) exotoxin production, which can cause widespread systemic symptoms in areas of the body where there are no organisms; and (3) immunologic, which occurs when antibody against a component of the organism cross-reacts with normal tissue or forms immune complexes that damage normal tissue (see the section on poststreptococcal diseases later in the chapter). The immunologic reactions cause inflammation (e.g., the inflamed joints of rheumatic fever), but there are no organisms in the lesions (Table 15–4).
Table 15–4Important Features of Pathogenesis by Streptococci ||Download (.pdf) Table 15–4 Important Features of Pathogenesis by Streptococci
|Organism ||Type of Pathogenesis ||Typical Disease ||Main Site of Disease (D), Colonization (C), or Normal Flora (NF) |
|S. pyogenes (group A) ||1. Pyogenic || || |
| a. Local ||Impetigo, cellulitis ||Skin (D) |
|Pharyngitis ||Throat (D) |
| b. Disseminated ||Sepsis ||Bloodstream (D) |
|2. Toxigenic ||Scarlet fever ||Skin (D) |
|Toxic shock ||Many organs (D) |
|3. Immune-mediated (poststreptococcal, nonsuppurative) || |
Heart, joints (D)
|S. agalactiae (group B) ||Pyogenic ||Neonatal sepsis and meningitis ||Vagina (C) |
|E. faecalis (group D) ||Pyogenic ||Urinary tract infection, endocarditis ||Colon (NF) |
|S. bovis (group D) ||Pyogenic ||Endocarditis ||Colon (NF) |
|S. pneumoniae ||Pyogenic ||Pneumonia, otitis media, meningitis ||Oropharynx (C) |
|Viridans streptococci ||Pyogenic ||Endocarditis ||Oropharynx (NF) |
The M protein of S. pyogenes is its most important antiphagocytic factor, but its capsule, composed of hyaluronic acid, is also antiphagocytic. Antibodies are not formed against the capsule because hyaluronic acid is a normal component of the body and humans are tolerant to it.
Group A streptococci produce four important enzymes related to pathogenesis:
Hyaluronidase degrades hyaluronic acid, which is the ground substance of subcutaneous tissue. Hyaluronidase is known as spreading factor because it facilitates the rapid spread of S. pyogenes in skin infections (cellulitis).
Streptokinase (fibrinolysin) activates plasminogen to form plasmin, which dissolves fibrin in clots, thrombi, and emboli. It can be used to lyse thrombi in the coronary arteries of heart attack patients.
DNase (streptodornase) degrades DNA in exudates or necrotic tissue. Antibody to DNase B develops during pyoderma; this can be used for diagnostic purposes. Streptokinase–streptodornase mixtures applied as a skin test give a positive reaction in most adults, indicating normal cell-mediated immunity.
IgG degrading enzyme is a protease that specifically cleaves IgG heavy chains. This prevents opsonization and complement activation thereby enhancing the virulence of the organism.
In addition, group A streptococci produce five important toxins and hemolysins:
Erythrogenic toxin causes the rash of scarlet fever. Its mechanism of action is similar to that of the TSST of S. aureus (i.e., it acts as a superantigen; see S. aureus, earlier, and Chapter 58). It is produced only by certain strains of S. pyogenes lysogenized by a bacteriophage carrying the gene for the toxin. The injection of a skin test dose of erythrogenic toxin (Dick test) gives a positive result in persons lacking antitoxin (i.e., susceptible persons).
Streptolysin O is a hemolysin that is inactivated by oxidation (oxygen-labile). It causes β-hemolysis only when colonies grow under the surface of a blood agar plate. It is antigenic, and antibody to it (ASO) develops after group A streptococcal infections. The titer of ASO antibody can be important in the diagnosis of rheumatic fever.
Streptolysin S is a hemolysin that is not inactivated by oxygen (oxygen-stable). It is not antigenic but is responsible for β-hemolysis when colonies grow on the surface of a blood agar plate.
Pyrogenic exotoxin A is the toxin responsible for most cases of streptococcal toxic shock syndrome. It has the same mode of action as does staphylococcal TSST (i.e., it is a superantigen that causes the release of large amounts of cytokines from helper T cells and macrophages; see Gram-Negative Bacteria and Memory T Cells).
Exotoxin B is a protease that rapidly destroys tissue and is produced in large amounts by the strains of S. pyogenes, the so-called “flesh-eating” streptococci that cause necrotizing fasciitis.
Pathogenesis by group B streptococci (S. agalactiae) is based on the ability of the organism to induce an inflammatory response. However, unlike S. pyogenes, no cytotoxic enzymes or exotoxins have been described, and there is no evidence for any immunologically induced disease. Group B streptococci have a polysaccharide capsule that is antiphagocytic, and anticapsular antibody is protective.
Pathogenesis by S. pneumoniae and the viridans streptococci is uncertain, as no exotoxins or tissue-destructive enzymes have been demonstrated. The main virulence factor of S. pneumoniae is its antiphagocytic polysaccharide capsule. Many of the strains of viridans streptococci that cause endocarditis produce a glycocalyx that enables the organism to adhere to the heart valve.
S. pyogenes causes three types of diseases: (1) pyogenic diseases such as pharyngitis and cellulitis, (2) toxigenic diseases such as scarlet fever and toxic shock syndrome, and (3) immunologic diseases such as rheumatic fever and acute glomerulonephritis (AGN). (See next section on poststreptococcal diseases.)
S. pyogenes (group A Streptococcus) is the most common bacterial cause of pharyngitis (sore throat). Streptococcal pharyngitis (strep throat) is characterized by throat pain and fever. On examination, an inflamed throat and tonsils, often with a yellowish exudate, are found, accompanied by tender cervical lymph nodes. If untreated, spontaneous recovery often occurs in 10 days, but rheumatic fever may occur (see next section on poststreptococcal diseases). Untreated pharyngitis may extend to the middle ear (otitis media), the sinuses (sinusitis), the mastoids (mastoiditis), or the meninges (meningitis). Continuing inability to swallow may indicate a peritonsillar or retropharyngeal abscess.
If the infecting streptococci produce erythrogenic toxin and the host lacks antitoxin, scarlet fever may result. A “strawberry” tongue is a characteristic lesion seen in scarlet fever. S. pyogenes also causes another toxin-mediated disease, streptococcal toxic shock syndrome, which has clinical findings similar to those of staphylococcal toxic shock syndrome (see Transmission). However, streptococcal toxic shock syndrome typically has a recognizable site of pyogenic inflammation and blood cultures are often positive, whereas staphylococcal toxic shock syndrome typically has neither a site of pyogenic inflammation nor positive blood cultures.
Group A streptococci cause skin and soft tissue infections, such as cellulitis, erysipelas (Figure 15–15), necrotizing fasciitis (streptococcal gangrene), and impetigo (see Figure 15–4).
Erysipelas. Note well-demarcated border of the inflamed area. Streptococcus pyogenes is the most common cause of erysipelas. (Reproduced with permission from Longo DL, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine, 18th ed. New York, NY: McGraw-Hill Education; 2012.)
Necrotizing fasciitis is often called the “flesh-eating” disease. In addition to S. pyogenes, Clostridium perfringens and MRSA are important causes. The clinical aspects of necrotizing fasciitis are described in Chapter 77.
Impetigo, a form of pyoderma, is a superficial skin infection characterized by “honey-colored” crusted lesions. Lymphangitis can occur, especially on the forearm associated with an infection on the hand.
Group A streptococci also cause endometritis (puerperal fever), a serious infection of pregnant women, and sepsis. Immune-mediated poststreptococcal AGN can also occur, especially following skin infections caused by certain M protein types of S. pyogenes.
Group B streptococci cause neonatal sepsis and meningitis. The main predisposing factor is prolonged (longer than 18 hours) rupture of the membranes in women who are colonized with the organism. Children born prior to 37 weeks of gestation have a greatly increased risk of disease. Also, children whose mothers lack antibody to group B streptococci and who consequently are born without transplacentally acquired IgG have a high rate of neonatal sepsis caused by this organism. Group B streptococci are an important cause of neonatal pneumonia as well.
Although most group B streptococcal infections are in neonates, this organism also causes infections such as pneumonia, endocarditis, arthritis, cellulitis, and osteomyelitis in adults. Postpartum endometritis also occurs. Diabetes is the main predisposing factor for adult group B streptococcal infections.
Viridans streptococci (e.g., S. mutans, S. sanguinis, S. salivarius, and S. mitis) are the most common cause of infective endocarditis. They enter the bloodstream (bacteremia) from the oropharynx, typically after dental surgery. Signs of endocarditis are fever, heart murmur, anemia, and embolic events such as splinter hemorrhages, subconjunctival petechial hemorrhages, and Janeway lesions. The heart murmur is caused by vegetations on the heart valve (see Figure 15–11). It is 100% fatal unless effectively treated with antimicrobial agents. About 10% of endocarditis cases are caused by enterococci, but any organism causing bacteremia may settle on deformed valves. At least three blood cultures are necessary to ensure recovery of the organism in more than 90% of cases.
Viridans streptococci, especially S. anginosus, S. milleri, and S. intermedius, also cause brain abscesses, often in combination with mouth anaerobes (a mixed aerobic–anaerobic infection). Dental surgery is an important predisposing factor to brain abscess because it provides a portal for the viridans streptococci and the anaerobes in the mouth to enter the bloodstream (bacteremia) and spread to the brain. Viridans streptococci are involved in mixed aerobic–anaerobic infections in other areas of the body as well (e.g., lung abscesses and abdominal abscesses, including liver abscesses).
Enterococci cause urinary tract infections, especially in hospitalized patients. Indwelling urinary catheters and urinary tract instrumentation are important predisposing factors. Enterococci also cause endocarditis, particularly in patients who have undergone gastrointestinal or urinary tract surgery or instrumentation. They also cause intra-abdominal and pelvic infections, typically in combination with anaerobes. S. bovis, a nonenterococcal group D Streptococcus, causes endocarditis, especially in patients with carcinoma of the colon. This association is so strong that patients with S. bovis, bacteremia, or endocarditis should be investigated for the presence of colonic carcinoma.
Peptostreptococci are one of the most common bacteria found in brain, lung, abdominal, and pelvic abscesses.
Poststreptococcal (Nonsuppurative) Diseases
These are disorders in which a local infection with group A streptococci is followed weeks later by inflammation in an organ that was not infected by the streptococci. The inflammation is caused by an immunologic (antibody) response to streptococcal M proteins that cross-react with human tissues. Some strains of S. pyogenes bearing certain M proteins are nephritogenic and cause AGN, and other strains bearing different M proteins are rheumatogenic and cause acute rheumatic fever. Note that these diseases appear several weeks after the actual infection because that is the length of time it takes to produce sufficient antibodies.
AGN typically occurs 2 to 3 weeks after skin infection by certain group A streptococcal types in children (e.g., M protein type 49 causes AGN most frequently). AGN is more frequent after skin infections than after pharyngitis. The most striking clinical features are hypertension, edema of the face (especially periorbital edema) and ankles, and “smoky” urine (due to red cells in the urine). Most patients recover completely. Reinfection with streptococci rarely leads to recurrence of glomerulonephritis.
The disease is initiated by antigen–antibody complexes on the glomerular basement membrane. Complement is activated and C5a attracts neutrophils that secrete enzymes that damage the endothelium of the glomerular capillaries. It can be prevented by early eradication of nephritogenic streptococci from skin colonization sites but not by administration of penicillin after the onset of symptoms.
Approximately 2 weeks after a group A streptococcal infection—usually pharyngitis—rheumatic fever, characterized by fever, migratory polyarthritis, and carditis, may develop. The carditis damages myocardial and endocardial tissue, especially the mitral and aortic valves, resulting in vegetations on the valves. Uncontrollable, spasmodic movements of the limbs or face (chorea) may also occur. ASO titers and the erythrocyte sedimentation rate are elevated. Note that group A streptococcal skin infections do not cause rheumatic fever. Most cases of pharyngitis caused by group A streptococci occur in children age 5 to 15 years, and hence rheumatic fever occurs in that age group.
Rheumatic fever is due to an immunologic cross-reaction between antibodies formed against M proteins of S. pyogenes and proteins on the surface of joint, heart, and brain tissue. It is an autoimmune disease greatly exacerbated by recurrent streptococcal infections. If streptococcal infections are treated within 8 days of onset, rheumatic fever is usually prevented. After a heart-damaging attack of rheumatic fever, reinfection must be prevented by long-term prophylaxis.
In the United States, less than 0.5% of group A streptococcal infections lead to rheumatic fever, but in developing tropical countries, the rate is higher than 5%. Rheumatic heart disease remains a significant global health burden.
Gram-stained smears are useless in streptococcal pharyngitis because viridans streptococci are members of the normal flora and cannot be visually distinguished from the pathogenic S. pyogenes. However, stained smears from skin lesions or wounds that reveal streptococci are diagnostic. Cultures of swabs from the pharynx or lesion on blood agar plates show small, translucent β-hemolytic colonies in 18 to 48 hours. If inhibited by bacitracin disk, they are likely to be group A streptococci (see Figure 15–14).
Group B streptococci are characterized by their ability to hydrolyze hippurate and by the production of a protein that causes enhanced hemolysis on sheep blood agar when combined with β-hemolysin of S. aureus (CAMP test). Group D streptococci hydrolyze esculin in the presence of bile (i.e., they produce a black pigment on bile-esculin agar). The group D organisms are further subdivided: the enterococci grow in hypertonic (6.5%) NaCl, whereas the nonenterococci do not.
Although cultures remain the gold standard for the diagnosis of streptococcal pharyngitis, a problem exists because the results of culturing are not available for at least 18 hours, and it is beneficial to know while the patient is in the office whether antibiotics should be prescribed. For this reason, rapid tests that provide a diagnosis in approximately 10 minutes were developed.
The rapid test detects bacterial antigens in a throat swab specimen. In the test, specific antigens from the group A streptococci are extracted from the throat swab with certain enzymes and are reacted with antibody to these antigens bound to latex particles. Agglutination of the colored latex particles occurs if group A streptococci are present in the throat swab. The specificity of these tests is high, but the sensitivity is low (i.e., false-negative results can occur). If the test result is negative but the clinical suspicion of streptococcal pharyngitis is high, a culture should be done.
A rapid test is also available for the detection of group B streptococci in vaginal and rectal samples. This PCR-based assay detects the DNA of the organism, and results can be obtained in approximately 1 hour.
Viridans group streptococci form α-hemolytic colonies on blood agar and must be distinguished from S. pneumoniae (pneumococci), which is also α-hemolytic. Viridans group streptococci are resistant to lysis by bile and will grow in the presence of optochin, whereas pneumococci will not. The various viridans group streptococci are classified into species by using a variety of biochemical tests.
ASO titers are high soon after group A streptococcal infections. In patients suspected of having rheumatic fever, an elevated ASO titer is typically used as evidence of previous infection because throat culture results are often negative at the time the patient presents with rheumatic fever. Titers of anti–DNase B are high in group A streptococcal skin infections and serve as an indicator of previous streptococcal infection in patients suspected of having AGN.
Group A streptococcal infections can be treated with either penicillin G or amoxicillin, but neither rheumatic fever nor AGN patients benefit from penicillin treatment after the onset of the two diseases. In mild group A streptococcal infections, oral penicillin V can be used. In penicillin-allergic patients, erythromycin or one of its long-acting derivatives (e.g., azithromycin) can be used. However, erythromycin-resistant strains of S. pyogenes have emerged that may limit the effectiveness of the macrolide class of drugs in the treatment of streptococcal pharyngitis. Clindamycin can also be used in penicillin-allergic patients. Streptococcal pyogenes is not resistant to penicillins.
Invasive group A streptococcal infections such as necrotizing fasciitis and streptococcal toxic shock syndrome can be treated with a combination of clindamycin and intravenous immunoglobulins.
Endocarditis caused by most viridans streptococci is curable using prolonged penicillin treatment. However, enterococcal endocarditis can be eradicated only by a penicillin or vancomycin combined with an aminoglycoside.
Enterococci resistant to multiple drugs (e.g., penicillins, aminoglycosides, and vancomycin) have emerged. Resistance to vancomycin in enterococci is mediated by a cassette of genes that encode the enzymes that substitute D-lactate for D-alanine in the peptidoglycan. The same set of genes encodes vancomycin resistance in S. aureus.
VREs are now an important cause of nosocomial infections; there is no reliable antibiotic therapy for these organisms. At present, two drugs are being used to treat infections caused by VRE: linezolid (Zyvox) and daptomycin (Cubicin).
Nonenterococcal group D streptococci (e.g., S. bovis) are not highly resistant and can be treated with penicillin G.
The drug of choice for group B streptococcal infections is either penicillin G or ampicillin. Some strains may require higher doses of penicillin G or a combination of penicillin G and an aminoglycoside to eradicate the organism. Peptostreptococci can be treated with penicillin G.
Rheumatic fever can be prevented by prompt treatment of group A streptococcal pharyngitis with penicillin G or oral penicillin V. Prevention of streptococcal infections (usually with benzathine penicillin once each month for several years) in persons who have had rheumatic fever is important to prevent recurrence of the disease. There is no evidence that patients who have had AGN require a similar penicillin prophylaxis.
In patients with damaged heart valves who undergo invasive dental procedures, endocarditis caused by viridans streptococci can be prevented by using amoxicillin perioperatively. To avoid unnecessary use of antibiotics, it is recommended to give amoxicillin prophylaxis only to patients who have the highest risk of severe consequences from endocarditis (e.g., those with prosthetic heart valves or with previous infective endocarditis) and who are undergoing high-risk dental procedures, such as manipulation of gingival tissue. It is no longer recommended that patients undergoing gastrointestinal or genitourinary tract procedures receive prophylaxis.
The incidence of neonatal sepsis caused by group B streptococci can be reduced by a two-pronged approach: (1) All pregnant women at 35 to 37 weeks of gestation should be screened by doing vaginal and rectal cultures. If cultures are positive, then penicillin G (or ampicillin) should be administered intravenously at the time of delivery. (2) If the patient has not had cultures done, then penicillin G (or ampicillin) should be administered intravenously at the time of delivery to women who have not delivered within 18 hours after rupture of membranes, or whose labor begins before 37 weeks of gestation, or who have a fever at the time of labor. If the patient is allergic to penicillin, either cefazolin or vancomycin can be used.
Oral ampicillin given to women who are vaginal carriers of group B streptococci does not eradicate the organism. Rapid screening tests for group B streptococcal antigens in vaginal specimens can be insensitive, and neonates born of antigen-negative women have, nevertheless, been diagnosed with neonatal sepsis. Note, also, that as group B streptococcal infections have declined as a result of these prophylactic measures, neonatal infections caused by E. coli have increased.
There are no vaccines available against any of the streptococci except S. pneumoniae (see following section).