Harrison’s Manual of Medicine



Streptococcal Infections

Group A Streptococcus (S. pyogenes)

Groups C and G Streptococci

Group B Streptococcus (GBS)

Group D Streptococcus

Viridans Streptococci
Enterococcal Infections
Outpatient/Home Care Considerations

Group A Streptococcus (S. pyogenes)
Streptococci of group A commonly cause pharyngitis as well as skin and soft tissue infection; they less often cause pneumonia, puerperal sepsis, and the postinfectious complications of acute rheumatic fever (ARF) and acute glomerulonephritis (AGN). Streptococci possess many virulence factors, including anti- phagocytic M proteins and a hyaluronic acid capsule, as well as a variety of extracellular toxins and enzymes, including pyrogenic toxins, streptolysins, streptokinase, and DNases.
PHARYNGITIS   Streptococcal pharyngitis is a common infection among children over age 3; streptococci account for 20–40% of all cases of exudative pharyngitis in children. This infection usually spreads from person to person via respiratory droplets, although other routes, including food-borne outbreaks, have been described. After an incubation period of 1–4 d, pts develop sore throat, fever, chills, and malaise and sometimes abdominal symptoms and vomiting. Both symptoms and signs are quite variable, ranging from mild with minimal findings to severe with markedly enlarged tonsils; a purulent exudate over the tonsils and posterior pharyngeal wall; and tender, enlarged cervical lymph nodes. The usual course of uncomplicated streptococcal pharyngitis lasts 3–5 d.
Scarlet fever, a group A streptococcal infection, usually takes the form of pharyngitis accompanied by a characteristic rash. In the past this infection was thought to occur in hosts who were not immune to one of the streptococcal pyrogenic exotoxins (A, B, or C). More recent studies suggest that the rash may be due to a hypersensitivity reaction requiring prior exposure to the toxin. The rash typically develops within 2 d of the sore throat; it begins on the neck, upper chest, and back and then spreads over the remainder of the body, sparing the palms and soles. This diffuse, blanching erythema with 1- to 2-mm punctate elevations has a “sandpaper” texture and is most intense along skin folds (Pastia’s lines). Circumoral pallor and a “strawberry tongue” (enlarged papillae on a coated tongue, which later becomes denuded) frequently accompany the rash. The rash subsides after 6–9 d and is followed by desquamation of the palms and soles.
Suppurative complications of streptococcal pharyngitis, uncommon since the widespread use of antibiotics, include acute otitis media, sinusitis, cervical lymphadenitis, peritonsillar or retropharyngeal abscess, meningitis, pneumonia, bacteremia and endocarditis. The most feared complications are the late nonsuppurative complications. ARF is a rare but serious disease that follows streptococcal pharyngitis. AGN (Chap. 142) may follow either pharyngitis or skin infection.
Diagnosis   Clinical criteria alone are unreliable for the diagnosis of streptococcal pharyngitis. Throat culture remains the “gold standard.” Rapid diagnostic kits are useful if the result is positive; however, because of low sensitivity, a negative result must be confirmed with a throat culture. Serologic tests such as antistreptolysin O confirm past infection in pts with suspected ARF or AGN but are not useful for the diagnosis of pharyngitis.

Treatment is given mainly to prevent ARF and must be started within 9 d of onset (Table 90-1).

Table 90-1 Treatment of Group A Streptococcal Infections

SKIN AND SOFT TISSUE INFECTION   Impetigo (Pyoderma)   Impetigo is a localized purulent skin infection that occurs predominantly in young children living in warm climates under conditions of poor hygiene. The usual sites of involvement are the face and lower extremities. Minor trauma may serve to inoculate the organisms into the skin. While it is usually due to group A streptococci, impetigo is occasionally caused by other streptococci or by Staphylococcus aureus. Papules become vesicular, with surrounding erythema, and form thick, honey-like crusts over 4–6 d. This infection is diagnosed by culture of the base of the lesion. Impetigo is not associated with ARF but frequently precedes AGN.

Agents active against both streptococci and S. aureus provide the most reliable therapy for impetigo. These drugs include dicloxacillin (500 mg PO qid), cephalexin (500 mg PO qid), and topical mupirocin ointment. If the infection is known to be due to group A streptococci, the regimens used for pharyngitis (Table 90-1) are cheaper and equally effective.

Cellulitis   Cellulitis, an infection of the skin and SC tissue, is caused by group A streptococci or S. aureus. The involved area is red, warm, and tender; fever and systemic symptoms often develop, and regional lymphadenopathy may be documented. Erysipelas is a form of cellulitis caused almost exclusively by group A streptococci and occasionally by group C or G organisms. It typically involves the face or lower extremities. There is an acute onset of pain and of a raised plateau of redness (formed by engorgement of lymphatic tissue) that is sharply demarcated from normal skin. Erysipelas may be associated with high fever and bacteremia.

Agents active against both streptococci and S. aureus provide the most reliable therapy for cellulitis. Therapy is initiated with oxacillin (2 g IV q4h) or cefazolin (2 g IV q8h); if the pt is allergic to penicillin or if methicillin-resistant S. aureus infection is suspected, vancomycin (1 g IV q12h) is used. If the infection is known to be due to group A streptococci, penicillin is preferred (Table 90-1).

Necrotizing Fasciitis   A rapidly life-threatening infection of the superficial or deep fascia, necrotizing fasciitis is caused by group A streptococci in 60% of cases. (Other cases, particularly those related to an abdominal or peritoneal process or surgery, are caused by bowel flora.) The onset of symptoms is acute and is marked by severe pain at the site of infection, malaise, fever, chills, and a toxic appearance. As the process evolves (often quite rapidly), skin changes become increasingly apparent, with dusky or mottled erythema; edema and anesthesia of the involved area may be noted. Surgical exploration is required both for confirmation of the diagnosis and for treatment. While antibiotic therapy (Table 90-1) is adjunctive, surgical debridement and resection are lifesaving.
PNEUMONIA AND EMPYEMA   Group A streptococci occasionally cause pneumonia, generally in previously healthy individuals. Pleuritic chest pain, fever, chills, and dyspnea are characteristic presenting symptoms, with either an abrupt or a gradual onset. Streptococcal pneumonia is accompanied by pleural effusion in 50% of cases, and the effusion is almost always infected. Treatment should include antibiotics and early drainage of the empyema (Table 90-1).
BACTEREMIA, PUERPERAL SEPSIS, AND STREPTOCOCCAL TOXIC SHOCK–LIKE SYNDROME   Bacteremia may complicate an identifiable local infection, particularly cellulitis, pneumonia, or necrotizing fasciitis. In the absence of a focus, evaluation for endocarditis, abscess, or osteomyelitis should be pursued. Occasionally, group A streptococci still cause endometritis and bacteremia complicating childbirth. Outbreaks of these infections have been associated with asymptomatic carriage of group A streptococci by delivery room personnel.
A toxic shock–like syndrome (see Table 140-3 in HPIM-15 for proposed case definition) has been described in association with group A streptococcal infections, especially necrotizing fasciitis, cellulitis, and myositis. This syndrome manifests as fever, hypotension, and multisystem organ failure and is associated with 30% mortality. In contrast to staphylococcal toxic shock syndrome, the streptococcal syndrome is usually characterized by the lack of a rash and by positive blood cultures.

Treatment of these infections requires aggressive supportive care, surgical debridement of involved local sites, and antibiotic administration. Data from experimental animals suggest that clindamycin (600 mg IV q6h) might be more effective than b-lactam antibiotics; however, there are currently no data on the treatment of humans with this regimen. Although clindamycin resistance in group A streptococci is uncommon, it has been documented. If clindamycin is used for initial treatment of a critically ill pt, penicillin (2–4 million U IV q4h) should be given as well until antibiotic susceptibility data are available for the isolate. The IV administration of immune globulin preparations has been used adjunctively in the treatment of streptococcal toxic shock syndrome, but no relevant controlled trials have been performed.

Groups C and G Streptococci
Streptococci of groups C and G cause infections similar to those caused by group A streptococci, including pharyngitis, bacteremia, pneumonia, cellulitis, soft tissue infection, septic arthritis, and endocarditis. Bacteremia involving these organisms tends to occur in elderly, debilitated, or chronically ill pts.

Appropriate therapy for adult infection consists of high-dose penicillin (18 million U/d) and aspiration or open debridement of infected joint spaces; for endocarditis or septic arthritis, gentamicin (1 mg/kg q8h) is added for synergy.

Group B Streptococcus (GBS)
NEONATAL INFECTIONS   GBS is the most frequent cause of neonatal sepsis and meningitis, with an incidence of 0.5–2 per 1000 births. (Escherichia coli is the second most frequent cause.) Early-onset infections become evident within 7 d of birth, with signs often present at birth. The infants involved most often present with respiratory distress, lethargy, and hypotension. Almost all are bacteremic, one-third to one-half have pneumonia or respiratory distress syndrome, and one-third have meningitis. Late-onset disease occurs between 1 week and 3 months after birth; generally presents as meningitis, occasionally with other focal infections or bacteremia; and is associated with a lower mortality rate than early-onset disease. Many meningitis survivors have neurologic sequelae. Infants with suspected neonatal sepsis should be treated with high- dose penicillin and gentamicin; penicillin may be given alone once GBS has been identified as the causative organism. Between 5 and 40% of women are identified by antenatal culture as carriers of GBS in the vagina or rectum. The CDC has suggested two strategies for the prevention of GBS infection in neonates. (1) Prenatal screening–based approach: Women are screened for colonization by swab culture of the lower vagina and rectum at 35–37 weeks of gestation. Intrapartum chemoprophylaxis should be offered to all carriers and is recommended for women with any risk factor (preterm delivery, rupture of membranes >24 h before delivery, prolonged labor, fever, chorioamnionitis, multiple gestation, or prior birth of an infant with GBS infection). (2) Risk factor–based approach: No screening is performed and intrapartum prophylaxis is recommended for all women with one or more of the risk factors just mentioned. The recommended regimen for prophylaxis is penicillin G (5 million U IV followed by 2.5 million U q4h until delivery), with clindamycin or erythromycin substituted in women who are allergic to penicillin.
ADULT INFECTIONS   Peripartum infections are the most common GBS infections in adults. The organism may cause puerperal sepsis, endometritis, or chorioamnionitis. Bacteremic cases may be complicated by meningitis or endocarditis. Other adult infections involve the elderly or those with other underlying conditions, such as diabetes mellitus or malignancy. These GBS infections include UTIs, diabetic skin ulcers, pneumonia, endocarditis, septic arthritis, intraabdominal abscesses, and osteomyelitis.

Appropriate treatment consists of penicillin G (12 million U/d IV). Meningitis and endocarditis should be treated with even higher doses (18–24 million U/ d IV in divided doses). Vancomycin (1 g IV q12h) may be substituted for penicillin in cases of allergy.

Group D Streptococcus
S. bovis is the main human pathogen among group D streptococci. Endocarditis due to S. bovis is associated with neoplasms and other lesions of the GI tract. In contrast to enterococci, S. bovis is highly susceptible to penicillin, which is the drug of choice for the infections it causes.
Viridans Streptococci
The viridans streptococci include multiple species of a-hemolytic streptococci. These organisms are part of the normal mouth flora and are the most frequent causative agents of bacterial endocarditis. Viridans streptococcal endocarditis may be treated with penicillin (12 million U/d). Occasional isolates characterized as nutritional variants (reclassified as Abiotrophia) require vitamin B6 for growth; against these isolates, gentamicin (1 mg/kg q8h) should be added for optimal coverage. The organisms of the S. milleri or S. intermedius group (S. intermedius, S. anginosus, and S. constellatus) are usually considered viridans streptococci but may be b-hemolytic and often cause suppurative infections such as intraabdominal or brain abscesses. These organisms are sensitive to penicillin, which is the drug of choice for treatment of the infections they cause. Viridans streptococcal bacteremia occurs with relatively high frequency among neutropenic pts with cancer and may cause a sepsis syndrome with high fever and shock. Risk factors include profound neutropenia, antibiotic prophylaxis with TMP-SMZ or fluoroquinolones, mucositis, and antacid/histamine antagonist therapy. In this setting, viridans streptococci are more commonly resistant to penicillin, and the infections they cause should be treated empirically with vancomycin (1 g IV q12h) pending susceptibility testing.
Previously classified as group D streptococci, enterococci are now recognized as a separate genus. Enterococcal infections tend to occur in pts who are elderly or debilitated or whose mucosal or skin barriers have been disrupted. Enterococci also cause superinfections in antibiotic-treated pts. Enterococcal infections most commonly involve the urinary tract, particularly in pts with anatomic abnormalities and in those who have undergone instrumentation. Enterococci account for 10–20% of cases of bacterial endocarditis. The presentation of enterococcal endocarditis is usually subacute but may also be acute with valvular destruction. Enterococci are frequently isolated from the biliary tract and may cause infections related to biliary surgery. Moreover, these organisms are often recovered in mixed infections from intraabdominal abscesses, surgical wounds, and diabetic foot ulcers.

While it is not always necessary to direct antimicrobial therapy at enterococci in mixed infections, these organisms should be covered by treatment when they are predominant or when they are present in blood cultures. Ampicillin (2 g IV q4h) is usually sufficient for the treatment of uncomplicated UTI. However, other types of enterococcal infection require penicillin or ampicillin and the addition of an aminoglycoside, usually gentamicin (1 mg/kg IV q8h with normal renal function), for synergy. Vancomycin (1 g q12h) may be substituted for penicillin in penicillin-allergic pts. Because of the increasing incidence of antibiotic resistance in enterococci (especially E. faecium), susceptibility testing should be performed for all isolates causing serious infections. Strains with high-level gentamicin resistance may be susceptible to other aminoglycosides or may respond to ampicillin alone. Infections due to enterococci that are resistant to penicillins on the basis of b-lactamase production may be treated with vancomycin, ampicillin/sulbactam, amoxicillin/ clavulanate, or imipenem in combination with an aminoglycoside. Moderately resistant enterococci (MIC of penicillin and ampicillin, 16–64 µg/mL) may be susceptible to high-dose penicillin or ampicillin in combination with gentamicin, but strains with MICs of ³200 µg/mL require treatment with vancomycin and gentamicin. Vancomycin-resistant enterococci, first reported in the late 1980s, have become common pathogens in many hospitals. For isolates resistant to both vancomycin and b-lactam antibiotics, there are no established therapies. Regimens that have been tried with some success include combinations such as ciprofloxacin/rifampin/gentamicin or ampicillin/vancomycin as well as chloramphenicol or tetracycline (if the strain is susceptible in vitro). Quinupristin/dalfopristin (Synercid) is a streptogramin with in vitro activity against E. faecium, including vancomycin-resistant isolates.

Persons with group A streptococcal pharyngitis and impetigo may be treated as outpatients with oral antibiotics. More serious infections, including cellulitis, mandate hospitalization and parenteral antibiotic therapy. Pts who exhibit a good response to parenteral antibiotic therapy (including resolution of signs of acute inflammation) may be switched to an oral regimen and complete their therapy as outpatients. Once their condition has stabilized, their fever has resolved, and their bacteremia has cleared, pts with viridans streptococcal endocarditis who show no signs of complications (such as embolization, heart block, or valvular failure) may complete their parenteral antibiotic therapy at home when this alternative is logistically feasible.
Diphtheria is a localized infection of mucous membranes or skin caused by Corynebacterium diphtheriae. Its incidence is increased among alcoholics, persons in lower socioeconomic groups, and Native Americans as well as under conditions of crowding. Its usual method of spread is by droplet. After an incubation period of 2–5 d, the illness manifests as low-grade fever and oropharyngeal pain, with the development of a thick gray membrane that covers the tonsils and pharynx and may extend over the larynx and cause airway obstruction. Dislodging of the membrane usually causes bleeding and occasionally causes obstruction of the respiratory tract. The major toxic manifestations of diphtheria are myocarditis and polyneuritis. Bulbar dysfunction develops in the first 2 weeks and peripheral polyneuritis in the 1–3 months after onset. Pneumonia occurs in more than half of fatal cases of diphtheria. Diagnosis of diphtheria of the respiratory tract is based on clinical suspicion; definitive diagnosis requires isolation of the organism. Cutaneous diphtheria may involve preexisting wounds, burns, or abrasions. A diagnosis is made by Gram’s staining of the lesion, which reveals characteristic club-shaped, gram-positive rods in palisades or a “Chinese character” configuration, or by culture of the organism on selective tellurite medium.

Treatment requires antitoxin, which must be administered in the following doses as early as possible after the diagnosis is suspected: for mild or early (£48 h) pharyngeal or laryngeal disease, 20,000–40,000 U; for nasopharyngeal involvement, 40,000–60,000 U; and for disease that is extensive, of ³3 d duration, or accompanied by diffuse swelling of the neck, 80,000–100,000 U. The pt should first be tested for hypersensitivity to horse serum, and the antiserum should then be administered IV in saline over 60 min. In addition, erythromycin (500 mg PO/IV qid for 14 d) or procaine penicillin G (600,000 units IM q12h) should be given for eradication of the organism in acute respiratory illness. Pts with cutaneous diphtheria and carriers can be treated with erythromycin (500 mg PO qid) or rifampin (600 mg PO qd) for a 7-d course. Diphtheria is preventable by immunization with DTaP or DT in childhood (for appropriate dosing schedule, see HPIM-15, Chap. 122) and reimmunization with Td every 10 years in adulthood.


For a more detailed discussion, see Wessels MR: Streptococcal and Enterococcal Infections, Chap. 140, p. 901; and Holmes RK: Diphtheria, Other Corynebacterial Infections, and Anthrax, Chap. 141, p. 909, in HPIM-15.



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