[Section Outline]
- Microbiology
- Group A Streptococcus (Gas)
- Streptococci of Groups C and G
- Group B Streptococcus (Gbs)
- Nonenterococcal Group D Streptococci
- Viridans Streptococci
- Abiotrophia and Granulicatella Species (Nutritionally Variant Streptococci)
- Enterococci
Streptococci and enterococci are gram-positive cocci that form chains when grown in liquid media.
- Culture on blood agar reveals three hemolytic patterns:
- - -Hemolysis results in partial hemolysis that imparts a greenish appearance to agar. This pattern is seen with S. pneumoniae and viridans streptococci.
- - -Hemolysis results in complete hemolysis around a colony. This pattern is seen with streptococci of Lancefield groups A, B, C, and G, which all form large (≥0.5-mm) colonies. Lancefield grouping is based on cell-wall carbohydrate antigens.
- - -Hemolysis describes the absence of hemolytic ability. This pattern is typical of enterococci, nonenterococcal group D streptococci, and anaerobic streptococci.
- Streptococci and enterococci colonize the respiratory, GI, and genitourinary tracts as part of the normal flora. Several of these species are also important causes of human diseases.
Epidemiology and Pathogenesis
GAS (S. pyogenes) causes suppurative infections and is associated with postinfectious syndromes such as acute rheumatic fever (ARF) and poststreptococcal glomerulonephritis (PSGN).
- Up to 20% of people may have asymptomatic pharyngeal colonization with GAS.
- Pharyngitis due to GAS is one of the most common bacterial infections of childhood.
- GAS accounts for 20-40% of all cases of exudative pharyngitis in children >3 years of age.
- The incidence of all GAS infections is ∼10-fold higher in low-income than in high-income countries. Worldwide, GAS contributes to ∼500,000 deaths per year.
- The major surface protein (M protein) and the hyaluronic acid polysaccharide capsule protect GAS against phagocytic ingestion and killing.
- GAS makes a large number of extracellular products that may contribute to local and systemic toxicity; these include streptolysins S and O, streptokinase, DNases, and the pyrogenic exotoxins that cause the rash of scarlet fever and contribute to the pathogenesis of toxic shock syndrome (TSS) and necrotizing fasciitis.
- Respiratory droplets provide the usual route of transmission, although other mechanisms have been described.
Clinical Manifestations
PHARYNGITIS- After an incubation period of 1-4 days, pts develop sore throat, fever, chills, malaise, and GI manifestations.
- Examination may reveal an erythematous and swollen pharyngeal mucosa, purulent exudates over the posterior pharynx and tonsillar pillars, and tender anterior cervical adenopathy.
- Viral pharyngitis is the more likely diagnosis when pts have cough, coryza, hoarseness, conjunctivitis, or mucosal ulcers.
- Throat culture is the gold standard for diagnosis.
- Latex agglutination or enzyme immunoassay is highly specific (>95%) and can be relied on for a rapid, definitive diagnosis.
- Given a variable sensitivity of 55-90%, a negative rapid-assay result should be confirmed with a throat culture.
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Gas Pharyngitis
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SCARLET FEVER- Scarlet fever is the designation for GAS infection-usually pharyngitis-associated with a characteristic rash. It is much less common now than in the past, although occasional outbreaks still occur.
- The rash typically appears over the upper trunk in the first 2 days of illness and spreads to the extremities but not to the palms and soles. The skin has a sandpaper feel.
- Other findings include circumoral pallor, strawberry tongue (enlarged papillae on a coated tongue), and Pastia's lines (accentuation of rash in skin folds).
- Rash improves in 6-9 days, with desquamation on palms and soles.
SKIN AND SOFT TISSUE INFECTIONS- See Chap. 87 Infections of the Skin, Soft Tissues, Joints, and Bones for further discussion of clinical manifestations and treatment.
- Impetigo: A superficial skin infection, impetigo is most often seen in young children in warmer months or climates and under poor hygienic conditions.
- Red papular lesions evolve into pustules that ultimately form characteristic honeycomb-like crusts, usually affecting the facial areas around the nose and mouth and the legs. Pts are usually afebrile.
- GAS impetigo is associated with PSGN but not with ARF.
- For treatment, see Table 90-1 Treatment of Group A Streptococcal Infections . Given an increasing incidence of impetigo due to Staphylococcus aureus, empirical antibiotic therapy should cover GAS and S. aureus.
- Thus dicloxacillin or cephalexin (250 mg PO qid for 10 days) is used.
- Topical mupirocin ointment is also effective.
- Cellulitis: GAS cellulitis develops at anatomic sites where normal lymphatic drainage has been disrupted (e.g., by surgery or prior cellulitis). When skin integrity is breached, organisms may enter at sites distant from the area of cellulitis.
- GAS may cause rapidly developing postoperative wound infections with a thin exudate.
- - Erysipelas is a form of cellulitis characterized by pain, fever, and acute onset of bright red swelling that is sharply demarcated from normal skin.
- It usually involves the malar facial area or the lower extremities and is caused almost exclusively by β-hemolytic streptococci, usually GAS.
- The skin often has a peau d'orange texture, and blebs or bullae may form after 2 or 3 days.
- For treatment of erysipelas or cellulitis known to be due to GAS, see Table 90-1 Treatment of Group A Streptococcal Infections ; empirical treatment should be directed against GAS and S. aureus.
- Necrotizing fasciitis: See Chap. 87 Infections of the Skin, Soft Tissues, Joints, and Bones for details. GAS causes ∼60% of cases of necrotizing fasciitis. For treatment, see Table 90-1 Treatment of Group A Streptococcal Infections .
PNEUMONIA AND EMPYEMA- GAS is an occasional cause of pneumonia in previously healthy pts.
- Pts have pleuritic chest pain, fever, chills, and dyspnea; ∼50% have accompanying pleural effusions that-unlike the sterile parapneumonic effusions of pneumococcal pneumonia-are almost always infected and should be drained quickly to avoid loculation.
- For treatment, see Table 90-1 Treatment of Group A Streptococcal Infections .
BACTEREMIA- In most adult cases of GAS bacteremia, a focus is readily identifiable. Bacteremia occurs occasionally with cellulitis or pneumonia and frequently with necrotizing fasciitis.
- If no focus is immediately evident, a diagnosis of endocarditis, occult abscess, or osteomyelitis should be considered.
TOXIC SHOCK SYNDROME- Unlike those with TSS due to S. aureus, pts with streptococcal TSS generally lack a rash, have bacteremia, and have an associated soft-tissue infection (cellulitis, necrotizing fasciitis, or myositis).
- Table 90-2 Proposed Case Definition for the Streptococcal Toxic Shock Syndromea presents a proposed case definition for streptococcal TSS.
- The mortality rate for streptococcal TSS is ≥30%, with most deaths due to shock and respiratory failure.
- For treatment, see Table 90-1 Treatment of Group A Streptococcal Infections .
Prevention
Although household contacts of individuals with invasive GAS infection are at increased risk of infection, the attack rate is low enough that antibiotic prophylaxis is not recommended. However, prophylaxis may be considered in unusually severe cases or for individuals at increased risk for invasive infection.
Streptococci of Groups C and G 
- Streptococci of groups C and G cause infections similar to those caused by GAS, including cellulitis, bacteremia (particularly in elderly or chronically ill pts), pneumonia, and soft tissue infections.
- Strains that form small colonies (<0.5 mm) on blood agar are generally of the S. milleri group (S. intermedius, S. anginosus); large-colony groups C and G streptococci are now considered a single species (S. dysgalactiae subsp. equisimilis).
- Treatment is the same as for similar syndromes due to GAS.
- Although it has not been shown to be superior, the addition of gentamicin (1 mg/kg IV q8h) is recommended by some experts for endocarditis or septic arthritis due to group C or G streptococci because of a poor clinical response to penicillin alone.
- Joint infections can require repeated aspiration or open drainage for cure.
- GBS is a major cause of meningitis and sepsis in neonates and a common cause of peripartum fever in women.
- About half of the infants delivered vaginally to mothers colonized with GBS (5-40% of women) become colonized, but only 1-2% develop infection.
- With maternal colonization, the risk of neonatal GBS infection is high if delivery is preterm or if the mother has an early rupture of membranes (>24 h before delivery), prolonged labor, fever, or chorioamnionitis.
- Widespread prenatal screening for GBS has reduced the incidence of neonatal infection to 0.6 case per 1000 live births; adults now account for a larger proportion of invasive GBS infections than do newborns.
Neonatal Infections
- Early-onset infection occurs within the first week of life (median age, 20 h). The infection is acquired within the maternal genital tract during birth.
- Neonates typically have respiratory distress, lethargy, and hypotension.
- Bacteremia is noted in ∼100% of cases, pneumonia in one-third to one-half, and meningitis in one-third.
- Late-onset infection develops in infants >1 week old and generally ≤3 months of age (mean age, 3-4 weeks). The organism is acquired during delivery or during later contact with a source.
- Meningitis is the most common manifestation.
- Infants present with lethargy, fever, irritability, poor feeding, and occasionally seizures.
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GBS Infections in Neonates
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- Prevention: Identification of high-risk mothers and prophylactic administration of ampicillin or penicillin during delivery reduce the risk of neonatal infection.
- Maternal screening for anogenital colonization with GBS at 35-37 weeks of pregnancy is currently recommended.
- Women who have previously given birth to an infant with GBS disease, who have a history of GBS bacteriuria during pregnancy, or who have an unknown culture status but risk factors noted earlier should receive intrapartum prophylaxis (usually 5 mU of penicillin G followed by 2.5 mU q4h until delivery).
- Cefazolin can be used for pts with a penicillin allergy who are at low risk for anaphylaxis.
- If the mother is at risk for anaphylaxis and the GBS isolate is known to be susceptible, clindamycin can be used; otherwise, vancomycin is indicated.
Infections in Adults
Most GBS infections in adults are related to pregnancy and parturition. Other GBS infections are seen in the elderly, especially pts with underlying conditions such as diabetes mellitus or cancer.
- Cellulitis and soft-tissue infection, UTI, pneumonia, endocarditis, and septic arthritis are most common.
- Penicillin (12 mU/d for localized infections and 18-24 mU/d for endocarditis or meningitis, in divided doses) is recommended. Vancomycin is an acceptable alternative for penicillin-allergic pts.
- Relapse or recurrent invasive infection occurs in ∼4% of cases.
Nonenterococcal Group D Streptococci
The main nonenterococcal group D streptococci that cause human infections are S. gallolyticus and S. infantarius (previously classified together as S. bovis), each of which has two subspecies.
- These organisms have been associated with GI malignancies and other bowel lesions, which are found in ≥60% of pts presenting with group D streptococcal endocarditis.
- Unlike enterococcal endocarditis, group D streptococcal endocarditis can be adequately treated with penicillin alone.
- Many viridans streptococcal species are part of the normal oral flora, residing in close association with the teeth and gingiva. Minor trauma such as flossing or toothbrushing can cause transient bacteremia.
- Viridans streptococci have a predilection to cause endocarditis. Moreover, they are often part of a mixed flora in sinus infections and brain and liver abscesses.
- Bacteremia is common in neutropenic pts, who can develop a sepsis syndrome with high fever and shock. Risk factors in these pts include chemotherapy with high-dose cytosine arabinoside, prior treatment with trimethoprim-sulfamethoxazole (TMP-SMX) or a fluoroquinolone, mucositis, or therapy with antacids or histamine antagonists.
- The S. milleri group (including S. intermedius, S. anginosus, and S. constellatus) differs from other viridans streptococci in both hemolytic pattern (i.e., they may be α-, β-, or γ;-hemolytic) and clinical syndromes. These organisms commonly cause suppurative infections, especially abscesses of brain and viscera, as well as infections of the oral cavity and respiratory tract such as peritonsillar abscess, empyema, and lung abscess.
- Neutropenic pts should receive vancomycin pending susceptibility testing; other pts may be treated with penicillin.
Abiotrophia and Granulicatella Species (Nutritionally Variant Streptococci)
- The organisms formerly known as nutritionally variant streptococci are now classified as Abiotrophia defectiva and three species within the genus Granulicatella. These fastidious organisms require media that are enriched (e.g., with vitamin B6) for growth.
- These organisms are more frequently associated with treatment failure and relapse in cases of endocarditis than are viridans streptococci. Thus, gentamicin (1 mg/kg q8h) must be added to the penicillin regimen.
Enterococci are gram-positive cocci that are observed as single cells, diplococci, or short chains.
- Enterococci share many morphologic and phenotypic characteristics with streptococci and thus were previously classified as the latter.
- Enterococci are generally nonhemolytic when cultured on blood agar plates.
- Enterococci are inherently resistant to a variety of commonly used antibiotics. Enterococcus faecium is the most resistant species, with >80% of U.S. isolates resistant to vancomycin (VRE) and >90% resistant to ampicillin. In contrast, resistance to vancomycin and ampicillin in E. faecalis isolates is much less common.
Although ≥18 enterococcal species have been isolated from human infections, E. faecalis and E. faecium cause the overwhelming majority of enterococcal infections.
- Enterococci are the second most common cause of nosocomial infection (after staphylococci), with roughly equal numbers of cases caused by E. faecalis and E. faecium.
- Colonization with VRE (as opposed to antibiotic-susceptible strains) predisposes to enterococcal infection. Risk factors for VRE colonization include prolonged hospitalization; long antibiotic courses; hospitalization in long-term care facilities, surgical units, and/or ICUs; organ transplantation; renal failure; high APACHE scores; and physical proximity to pts colonized with VRE.
Enterococci cause UTIs, especially in pts who have undergone instrumentation and in those with chronic prostatitis, bacteremia related to intravascular catheters, bacterial endocarditis of both native and prosthetic valves (usually with a subacute presentation), meningitis (particularly after neurosurgery), soft-tissue infections (particularly involving surgical wounds), and neonatal infections. These organisms can also be a component of mixed intraabdominal infections.
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Enterococcal Infections
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