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Group B Streptococcus (S Agalactiae) Clinical Syndromes


Early-onset group B streptococcal neonatal infection has three major clinical expressions: bacteremia with no identifiable focus of infection, pneumonia, and meningitis (Box 1). Signs and symptoms of early-onset group B streptococcal neonatal infection include lethargy, poor feeding, jaundice, abnormal temperature, grunting respirations, pallor, and hypotension.

In most infants with pneumonia, symptoms of respiratory distress are present at or within a few hours after birth. Signs of respiratory distress associated with pneumonia include apnea, grunting, tachypnea, and cyanosis. The radiographic findings in infants with pneumonia may be indistinguishable from those of hyaline membrane disease.


Infants with meningitis have a clinical presentation that initially cannot be distinguished from that of infants without meningeal invasion. Lumbar puncture is required to identify neonates with meningitis.

The mortality of early-onset group B streptococcal infection is 10-15% but may be higher in infants with lower birth weights. One-half of patients with meningitis develop seizures within 24 hours of onset; if seizures persist, a poor outcome may follow.


The mean age of onset of late-onset group B streptococcal neonatal infection is 24 days. Bacteremia with concomitant meningitis is a frequent presentation. Signs and symptoms include poor feeding, irritability, and fever. Some infants present with fulminant infection characterized by progression within a few hours from the absence of symptoms to a morbid state with septic shock and seizures with cerebrospinal fluid Gram stains demonstrating sheets of organisms. This fulminant presentation is associated with an increased risk for mortality or permanent neurologic sequelae. Neutropenia on admission, prolonged seizures, and high concentrations of polysaccharide antigen in admission cerebrospinal fluid specimens are also associated with fatal outcomes or permanent neurologic sequelae.

Of all survivors of early- or late-onset group B streptococcal meningitis, 25% to 50% will have permanent neurologic sequelae. One-third of patients with these complications will have severe blindness, deafness, and/or global developmental delay. In the remainder of patients, the deficits are subtler and may be detectable only when language and cognitive function are adequately tested.

Bacteremia without an apparent focus and bone and joint infections are other clinical presentations of late onset group B streptococcal disease. Infants with bacteremia should be evaluated for foci of infection including cellulitis, adenitis, otitis media, conjunctivitis, peritonitis, endocarditis, or deep abscesses. Group B streptococcal osteomyelitis is characterized by an indolent onset in which diminished movement of the involved extremity is the most common symptom. Septic arthritis is associated with an acute onset of symptoms usually in the context of bacteremia. Fever is uncommon in both bone and joint infections. Lower extremity involvement is most commonly observed in patients with septic arthritis, whereas osteomyelitis has a predilection for involvement of the proximal humerus. However, involvement of the femur, tibia, and flat and small bones may be seen.


Group B streptococci cause symptoms of endometritis including fever, malaise, and moderate uterine tenderness. Pelvic abscesses, septic shock, and septic thrombophlebitis are rarely seen. Group B streptococci also cause peripartum bacteriuria that may be asymptomatic or may be diagnosed in association with cystitis or, less frequently, pyelonephritis.


This may occur in patients with diabetes mellitus or neurologic disease. Chest radiographs may demonstrate bilateral or lobar infiltrates. Infection is frequently polymicrobial, although group B streptococci are usually the predominant organisms. Empyema may be present.


Endocarditis caused by group B streptococci is rare. The mitral valve is more frequently involved than the aortic valve, and tricuspid valve involvement is found mainly in intravenous drug users. Underlying heart disease is present in more than one-half of cases, and rheumatic heart disease is the most common underlying condition. Valvular disease, atherosclerotic heart disease, and mitral valve prolapse have also been described as predisposing factors. Large friable vegetations are a frequent feature of group B streptococcal endocarditis. Embolization may occur early. Rapid valvular destruction may occur necessitating early valve replacement in some patients.


This is typically monoarticular and most commonly affects the knee, hip, or shoulder joints (see site). Diabetes mellitus is a predisposing factor, as are osteoarthritis and the presence of a prosthetic joint. The most common presenting signs are fever and joint pain in a patient with septicemia. Osteomyelitis may occur as a consequence of adjacent arthritis, peripheral vascular disease, orthopedic surgery, or concomitant infections such as frontal sinusitis. Hematogenously acquired osteomyelitis is most likely to involve the vertebrae. Osteomyelitis may complicate foot ulcers in adults with long-standing diabetes mellitus. In patients with prosthetic joints, group B streptococci typically cause acute onset septic arthritis with local pain, erythema, and swelling.


Group B streptococci may cause cellulitis, foot ulcers, abscesses, and infection of decubitus ulcers (see site).


Meningitis, keratitis, endophthalmitis, urinary tract infections in nonobstetric populations, and other unusual presentations may also occur.


The diagnosis of group B streptococcal infection is made by the isolation of the organism from typically sterile sites (eg, blood, cerebrospinal fluid, abscess material). Antigen detection methods may be used to permit a presumptive diagnosis, especially in neonates. Countercurrent immunoelectrophoresis, latex agglutination, staphylococcal coagglutination, and enzyme immunoassays may be used to detect group B streptococcal antigen in various body fluids. A number of selective media enhance the accurate detection by culture of low numbers of group B streptococci from sites such as the genital or gastrointestinal tract of pregnant women. These media usually contain Todd-Hewitt broth with or without sheep red blood cells and antimicrobial agents such as nalidixic acid and gentamicin or colistin. Molecular and antigen detection methods can also be used to detect group B streptococcal genital or gastrointestinal tract colonization in pregnant women.


Group B streptococci are uniformly susceptible to penicillin, although less so than S pyogenes. Penicillin G is therefore the drug of choice; however, because of the increased penicillin MIC (as compared with S pyogenes), the combination of penicillin plus an aminoglycoside is recommended for the treatment of group B streptococcal endocarditis (Box 2). Penicillin plus an aminoglycoside exhibit in vitro and in vivo synergistic killing of the organism. Group B streptococci are also susceptible to ampicillin, imipenem, vancomycin, and first-, second- (excluding cefoxitin), and third-generation cephalosporins, although degrees of activity vary. Some isolates are resistant to clindamycin, erythromycin, and clarithromycin; tetracycline resistance is frequently seen. Group B streptococci are uniformly resistant to nalidixic acid, trimethoprim-sulfamethoxazole, and aminoglycosides.

Parenteral therapy of a 10-day duration is recommended for treatment of bacteremia, pneumonia, pyelonephritis, and soft tissue infections, whereas a 14-day minimum duration is recommended for treatment of meningitis and a 4-week minimum for treatment of endocarditis or ventriculitis. In adults with endocarditis, cardiac surgery early in the course may be necessary because of rapid left-sided valvular destruction. In practice, many neonates are empirically treated with ampicillin plus gentamicin.

Prevention & Control

Prevention of early onset neonatal sepsis and postpartum maternal febrile morbidity may be achieved by administration of intravenous ampicillin or penicillin during labor. Women colonized with group B streptococci may be identified by obtaining cultures using lower vaginal and anorectal swabs processed in selective broth media or by using rapid antigen or molecular detection methods when patients are admitted to the hospital. The American College of Obstetrics and Gynecology, the American Academy of Pediatrics, and the Centers for Disease Control and Prevention have developed two strategies (a screening approach and a nonscreening approach) for preventing perinatal group B streptococcal disease (Box 3).

To prevent early onset sepsis, maternal chemoprophylaxis should be initiated at least 4 h before delivery and at high doses (see Box 3). This allows time to achieve sufficient concentrations of ampicillin or penicillin in the fetal circulation and in the amniotic fluid. Management of neonates born to women receiving chemoprophylaxis should be based on clinical findings.

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