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(See also Gram-Positive Cocci: Pneumococcal Infections; see Rheumatic Fever; see Oropharyngeal Disorders: Tonsillopharyngitis.)
Streptococci
are gram-positive aerobic organisms that cause many disorders, including
pharyngitis, pneumonia, wound and skin infections, sepsis, and endocarditis.
Symptoms vary with the organ infected. Sequelae include rheumatic fever
and glomerulonephritis. Clinical diagnoses are confirmed by Gram
stain and culture. Most strains are sensitive to penicillin, with
the exception of enterococci, which can be resistant to multiple
drugs. Recently, erythromycin-resistant strains have emerged.
Three different types of streptococci are initially differentiated by their appearance when grown on sheep blood agar. β-Hemolytic streptococci produce zones of clear hemolysis around each colony, α-hemolytic streptococci (including viridans group streptococci) are surrounded by green discoloration resulting from incomplete hemolysis, and γ-hemolytic streptococci are nonhemolytic. Subsequent classification, based on carbohydrates present in the cell wall, divides streptococci into the Lancefield groups A through H and K through T (see Table 2: Gram-Positive Cocci: Classification of Streptococci ). Viridans streptococci form a separate group that is difficult to classify. In the Lancefield classification, enterococci were initially included among the group D streptococci. More recently, enterococci have been classified as a separate genus.
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Table 2
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Classification of Streptococci
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Lancefield Group
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Species
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Hemolysis
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Associated Diseases
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Treatment
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A
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S. pyogenes
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β
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Pharyngitis, tonsillitis, wound and skin infections, septicemia, scarlet fever, pneumonia, rheumatic fever, glomerulonephritis
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Penicillin, erythromycin , clindamycin
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Necrotizing fasciitis
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Expeditious surgical management. β-Lactam (usually broad spectrum until etiology is identified; if GABHS is confirmed, can use penicillin or cefazolin ) plus clindamycin
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B
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S. agalactiae
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β
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Sepsis, postpartum or neonatal sepsis, skin infections, endocarditis, septic arthritis
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Penicillin or ampicillin ; cephalosporin; vancomycin
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C and G
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S. equi,
S. canis
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β
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Pharyngitis, pneumonia, cellulitis, pyoderma, erysipelas, impetigo, wound infections, puerperal sepsis, neonatal sepsis, endocarditis, septic arthritis
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Penicillin, vancomycin , cephalosporins, macrolides (variable susceptibility)
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D
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Enterococcal: E. faecalis, E. durans, and
E. faecium
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α or γ
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Endocarditis, UTI, intra-abdominal infection, cellulitis, and wound infection as well as concurrent bacteremia
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Enterococci: penicillin, ampicillin , or vancomycin (plus an aminoglycoside if serious infection)
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Nonenterococcal:
S. bovis and S. equinus
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Vancomycin -resistant enterococci: Streptogramins, oxazolidinones
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Viridans*
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S. mutans,
S. sanguis, S. salivarius, S. mitior,
A. milleri
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α or γ
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Endocarditis, localized infection or abscesses
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Penicillin, other based on in vitro susceptibility
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S. iniae
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Cellulitis and invasive infections from fish
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Penicillin
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*Do not conform to specific serogroups.
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GABHS = Group A β-hemolytic streptococci.
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Many streptococci elaborate virulence factors, including streptolysins, DNases, and hyaluronidase, which contribute to tissue destruction and spread of infection. A few strains release exotoxins that activate certain T cells, triggering release of cytokines, including tumor necrosis factor-α, interleukins, and other immunomodulators, which activate the complement, coagulation, and fibrinolytic systems, in turn leading to shock, organ failure, and death.
Streptococcal
Diseases
The most significant streptococcal pathogen is S. pyogenes, which is β-hemolytic and in Lancefield Group A, thus denoted as group A β-hemolytic streptococci (GABHS). The 2 most common acute diseases due to GABHS are pharyngitis and skin infections; in addition, delayed, nonsuppurative complications (rheumatic fever and acute glomerulonephritis) sometimes occur ≥ 2 wk after infection. Disease caused by other streptococcal species is less prevalent, and usually involves soft-tissue infection or endocarditis (see Table 2: Gram-Positive Cocci: Classification of Streptococci). Some non-GABHS infections occur predominantly in certain populations (eg, group B streptococci in neonates and postpartum women, enterococci in hospitalized patients).
Infections can spread through the affected tissues and along lymphatic channels to regional lymph nodes. They also can produce local suppurative complications, such as peritonsillar abscess, otitis media, sinusitis, and bacteremia. Suppuration depends on the severity of infection and the susceptibility of tissue.
Streptococcal pharyngitis is usually caused by GABHS. About 20% of patients present with sore throat, fever, a beefy red pharynx, and a purulent tonsillar exudate. The remainder have less prominent symptoms, and the examination resembles that of viral pharyngitis. The cervical and submaxillary nodes may enlarge and become tender. Streptococcal pharyngitis can lead to peritonsillar abscess (see Oropharyngeal Disorders: Peritonsillar Abscess and Cellulitis). Cough, laryngitis, and stuffy nose are uncharacteristic of streptococcal pharyngeal infection; their presence suggests another cause (usually viral or allergic). An asymptomatic carrier state may exist in as many as 20%.
Scarlet fever is uncommon today. Scarlet fever is caused by group A streptococcal (and occasionally other) strains that produce an erythrogenic toxin, leading to a diffuse pink-red cutaneous flush that blanches on pressure. The rash is seen best on the abdomen or the lateral chest, as dark red lines in skin folds (Pastia's lines), or as circumoral pallor. A strawberry tongue (inflamed papillae protruding through a bright red coating) also occurs and must be differentiated from that seen in toxic shock syndrome (see Gram-Positive Cocci: Toxic Shock Syndrome (TSS)) and Kawasaki disease (see Bone and Connective Tissue Disorders in Children: Slipped Capital Femoral Epiphysis (SCFE)). The upper layer of the previously reddened skin often desquamates after fever subsides. Other symptoms are similar to those in streptococcal pharyngitis, and the course and management of scarlet fever are the same as for other group A infections.
Skin infections include impetigo (see Bacterial Skin Infections: Impetigo and Ecthyma) and cellulitis (see Bacterial Skin Infections: Cellulitis). Cellulitis may spread rapidly due to the numerous lytic enzymes and toxins produced mainly by group A streptococcus. Erysipelas (see Bacterial Skin Infections: Erysipelas) is a particular form of streptococcal cellulitis.
Necrotizing fasciitis due to S. pyogenes is a severe dermal (or rarely muscular) infection that spreads along fascial planes (see Bacterial Skin Infections: Necrotizing Subcutaneous Infection). The inoculation originates through the skin or bowel, and the defect may be surgical, trivial, distant from the disease site, or occult, as with colonic diverticula or an appendiceal abscess. It is prevalent among IV drug abusers. Formerly known as streptococcal gangrene and popularized as the “flesh-eating bacteria,” the same syndrome also may be polymicrobial, involving a host of aerobic and anaerobic flora, including Clostridium perfringens. When it occurs in the perineum it is called Fournier's gangrene. Comorbid conditions, such as impaired immunity, diabetes, and alcoholism, are common. Symptoms begin with fever and exquisite localized pain. Thrombosis of the microvasculature causes ischemic necrosis, leading to rapid spread and disproportionally severe toxicity. In 20 to 40% of cases, adjacent muscles are invaded. Shock and renal dysfunction are common. Mortality is high, even with treatment.
Septicemia, puerperal sepsis, endocarditis, and pneumonias due to streptococci remain serious complications, especially if the organism is a multiresistant enterococcus.
Streptococcal toxic shock syndrome (see Gram-Positive Cocci: Toxic Shock Syndrome (TSS)), similar to that caused by S. aureus, may result from toxin-producing strains of GABHS. Patients are usually otherwise healthy children or adults with skin and soft-tissue infections.
Delayed complications:
The mechanism by which certain strains of GABHS cause delayed complications is unclear but may involve cross-reactivity of streptococcal antibodies against host tissue.
Rheumatic fever (see Rheumatic Fever), an inflammatory disorder, occurs in < 3% of patients in the weeks after untreated GABHS upper respiratory tract infection. It is much less common today than in the pre-antibiotic era. Diagnosis depends on a combination of arthritis, carditis, chorea, specific cutaneous manifestations, and laboratory tests. The most important reason for treating strep throat is to prevent rheumatic fever.
Poststreptococcal acute glomerulonephritis (see Glomerular Diseases: Rapidly Progressive Glomerulonephritis (RPGN)) is an acute nephritic syndrome following pharyngitis or skin infection from certain nephritogenic strains of GABHS. This sequela follows infection with a limited number of group A streptococcal serotypes. The overall attack rate after a throat or skin infection with it is about 10 to 15%. It is most common in children, occurring 1 to 3 wk after infection. Nearly all children, but somewhat fewer adults, recover without permanent renal damage. Antibiotic treatment of GABHS infection has little effect on development of glomerulonephritis.
Diagnosis
Streptococci are readily identified by culture on a sheep blood agar plate. Rapid antigen-detection tests are available that allow detection of GABHS directly from throat swabs. Many tests are based on enzyme immunoassay methodology; but more recently, tests using optical immunoassay have become available. They have high specificity (> 95%) but vary considerably in sensitivity (55% to 80 to 90% for the newer optical immunoassay test). Negative results should be confirmed by culture (particularly if a macrolide is being considered because of potential resistance).
During convalescence, evidence of infection can be obtained indirectly by demonstrating antistreptococcal antibodies in serum. Antibodies are most useful in diagnosis of post-streptococcal diseases, such as rheumatic fever and glomerulonephritis. Confirmation requires that sequential specimens show a rise in titer, because a single value may be high from a long antecedent infection. Serum specimens need not be taken more often than q 2 wk and may be taken q 2 mo. A significant rise (or fall) in titer should span at least 2 serial dilutions. The antistreptolysin O (ASO) titer rises in only 75 to 80% of infections. For completeness in difficult cases, any one of the other tests (antihyaluronidase, antideoxyribonuclease B, antinicotinamide adenine dinucleotidase, or antistreptokinase) also can be used. Penicillin given within the first 5 days for symptomatic streptococcal pharyngitis may delay the appearance and decrease the magnitude of the ASO response. Patients with streptococcal pyoderma usually do not have a significant ASO response but may have a response to other antigens (ie, anti-DNase or antihyluronidase).
Treatment
Pharyngitis:
(See also the Infectious Diseases Society of America's Practice
Guidelines for the Diagnosis and Management of Group A Streptococcal
Pharyngitis.) Pharyngeal GABHS infections, including scarlet fever, ordinarily are self-limited. Antibiotics shorten the course in young children, especially those with scarlet fever, but have only modest effect on symptoms in adolescents and adults. However, they help prevent local suppurative complications and rheumatic fever.
Penicillin is the drug of choice. A single injection of benzathine penicillin G , 600,000 units IM for small children (< 27.3 kg) or 1.2 million units IM for adolescents and adults usually suffices. Oral penicillin V may be used if the patient can be trusted to maintain the regimen for the required 10 days; 500 mg of penicillin V bid or tid (250 mg for children < 27 kg) is given. Oral cephalosporins are effective. Cefdinir , cefpodoxime , and azithromycin can be used for a 5-day course of therapy. Delaying treatment 1 to 2 days until laboratory confirmation increases neither the duration of disease nor the incidence of complications.
When penicillin or a β-lactam is contraindicated, erythromycin 250 mg po qid or clindamycin 300 mg po tid may be given for 10 days, although resistance of GABHS to macrolides has been detected (some authorities recommend confirmation of in vitro susceptibility if a macrolide is to be used and there is the possibility of macrolide resistance in the community). TMP-SMX, some of the fluoroquinolones, and the tetracyclines are unreliable. Clindamycin (5 mg/kg po qid) is preferred in children who have relapses of chronic tonsillitis, possibly because of its good activity against penicillinase-producing staphylococci or anaerobes coinfecting the tonsillar crypts and inactivating penicillin G . Clindamycin also appears to halt exotoxin production more rapidly than other agents.
Sore throat, headache, fever can be treated with analgesics or antipyretics. Bed rest and isolation are unnecessary. Close contacts who are symptomatic or have a history of post-streptococcal complications should be examined for streptococci.
Skin
infection:
Cellulitis is often treated without performing a culture because isolating organisms can be difficult. Thus regimens effective against both streptococci and staphylococci are used (see Bacterial Skin Infections: Treatment). Necrotizing fasciitis should be treated in an ICU. Extensive (perhaps repeated) surgical debridement is required. A recommended initial antibiotic regimen is a β-lactam (often a broad-spectrum agent until the etiology is confirmed by culture) plus clindamycin . Although streptococci remain susceptible to β-lactam antibiotics, animal studies have shown that penicillin is not always effective with a large bacterial inoculum because the streptococci are not rapidly growing.
Other streptococcal
infections:
Drugs of choice for treating group B, C, and G infections are penicillin, ampicillin , or vancomycin . Cephalosporins or macrolides are generally effective, but susceptibility tests must guide therapy, especially in very ill, immunocompromised, or debilitated hosts and in people with foreign bodies at the infection site. Surgical wound drainage and debridement as adjuncts to antimicrobial therapy may be lifesaving.
S.
bovis is relatively susceptible to antibiotics. Although vancomycin -resistant S.
bovis isolates recently have been reported, the organism remains susceptible to penicillin and aminoglycosides.
Most viridans streptococci are often susceptible to penicillin G and other β-lactams. Resistance is growing, and therapy for such strains should be dictated by results of in vitro susceptibility tests.
Enterococcal
Infections
Enterococcus
faecalis and E. faecium cause endocarditis, UTI, intra-abdominal infection, cellulitis, and wound infection as well as concurrent bacteremia. Enterococci associated with serious infections are difficult to eradicate unless a combination of a cell wall–active drug, such as penicillin, ampicillin , or vancomycin , plus an aminoglycoside, such as gentamicin or streptomycin , is used.
Vancomycin -resistant enterococci (VRE) also may be resistant to aminoglycosides, cell wall–active β-lactams (such as penicillin G and ampicillin ), and other glycopeptides (such as teicoplanin). When identified, strict isolation techniques should be used. Recommended treatment includes streptogramins (quinupristin plus dalfopristin) and oxazolidinones ( linezolid ).
Last full review/revision November 2005
Content last modified February 2008
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