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Streptococcus Group B Infections

  • Author: Christian J Woods, MD, FCCP; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 20, 2015
 

Practice Essentials

Group B Streptococcus (GBS), also known as Streptococcus agalactiae, is best known as a cause of postpartum infection and as the most common cause of neonatal sepsis. This organism is also causes infection in nonpregnant adults. Group B streptococcal infection in healthy adults is extremely uncommon, except in young and middle-aged women, and is almost always associated with underlying abnormalities, with diabetes most commonly associated with infection in some series.

Signs and symptoms

The GBS organism colonizes the vagina, GI tract, and the upper respiratory tract of healthy humans. GBS infection is almost always associated with underlying abnormalities. In elderly persons aged 70 years or older, GBS infection is strongly linked with congestive heart failure and being bedridden.

Signs and symptoms of GBS infection include the following:

  • GBS pneumonia: Rare with few unique features; observed in elderly people with diabetes and with neurologic deficits; fever, shortness of breath, chest pain, pleuritic pain, or cough
  • GBS meningitis: Common manifestation of neonatal infection; uncommon in adults; almost always associated with anatomical abnormalities contiguous with, or of, the CNS, usually as a result of neurosurgery; fever, headache, nuchal rigidity, or confusion
  • GBS bacteremia: Common; most cases have no identifiable source of infection; fever, malaise, confusion, chest pain, shortness of breath, myalgia, or arthralgia
  • Skin and soft-tissue infection, decubitus ulcers, colonization of diabetic foot infections: Fever, malaise, localized pain, cellulitis
  • Osteomyelitis, arthritis, discitis: Fever, malaise, localized pain, cellulitis, arthralgia, arthritis, or weakness
  • Chorioamnionitis, endometritis, UTIs (from asymptomatic bacteruria to cystitis and pyelonephritis with bacteremia): Fever, dysuria, flank pain, or pelvic pain

See Clinical Presentation for more detail.

Diagnosis

Examination in patients with GBS infection may demonstrate the following findings:

  • Lung consolidation, pleural effusion
  • Tachypnea
  • Tachycardia, murmur, evidence of heart failure
  • Hypotension
  • Headache, nuchal rigidity
  • Confusion, altered mental status, neurologic dysfunction
  • Evidence of an embolic event, phlebitis,
  • Splenomegaly
  • Vascular insufficiency of the lower extremity, wound infection
  • Back, flank, pelvic, or abdominal pain

Lab tests

Laboratory studies in a patient with suspected GBS infection may include the following:

  • Gram stain
  • Isolation of GBS from blood, CSF, and/or a site of local suppuration: The only method for diagnosing invasive GBS infection
  • GBS antigen detection in blood, CSF, and/or urine

Imaging tests

The following imaging studies may be obtained in a patient suspected of having GBS infection:

  • Chest radiography: May show pneumonia in elderly bedridden patient with fever, neurologic deficits, or other appropriate symptoms; infiltrate or effusion may be seen
  • Radiography of an affected region in a patient who is elderly, bedridden, or diabetic with fever and appropriate symptoms: May reveal evidence of gas or bone destruction in such patients with soft-tissue infection, osteomyelitis, discitis, epidural abscess, wound infection, necrotizing fasciitis, decubitus ulcer
  • CT scanning of an affected region: May reveal phlegmon, abscess, or osteomyelitis
  • CT scanning of the head in the neurosurgical patient with fever and other appropriate symptoms: May show meningitis; may reveal an abscess or contiguous infection
  • Echocardiography in a patient with fever of unclear source: May demonstrate vegetation or evidence of valve destruction
  • Ultrasonography of the GU system or pelvis in a postpartum woman or older man or woman with fever and appropriate symptoms: May reveal evidence of GU obstruction or abscess
  • CT scanning and MRIs of the GU system or pelvis: May show evidence of obstruction or abscess

Procedures

The following are procedures that may be performed in cases of suspected GBS infection:

  • Lumbar puncture for suspected GBS meningitis: First, exclude increased intracranial pressure with CT scanning, then perform LP
  • Diagnostic and therapeutic thoracentesis in GBS pneumonia: In the presence of pleural effusion; empyema requires drainage by thoracentesis, chest tube, or surgery
  • Valve replacement in GBS bacteremia, endocarditis, and line-related sepsis: Due to destructive endocarditis
  • Diagnostic aspiration and curative surgery: For GBS soft-tissue infection, arthritis, osteomyelitis, discitis, and epidural abscess
  • Diagnostic aspiration/tap with ultrasonography or CT-scan guidance in UTI or pelvic abscess: To isolate the organism, relieve obstruction, or drain an abscess

See Workup for more detail.

Management

Pharmacotherapy

GBS infection is primarily managed with antibiotics, including the following:

  • Penicillin G: Drug of choice for GBS infection
  • Ampicillin: Also a drug of choice for GBS infection
  • Vancomycin: The initial treatment of choice for GBS infection in patients who are allergic to penicillin (owing to possible resistance with clindamycin)
  • Clindamycin: Obtain sensitivity testing because of increasing resistance; PO clindamycin remains an excellent agent to follow a course of parenteral therapy for bone, soft-tissue, and lung infections if the isolate is susceptible
  • Cefazolin: Alternative therapy to penicillin for GBS infection; not effective for GBS meningitis
  • Telavancin: For complicated skin and skin structure infections caused by susceptible gram-positive bacteria, such as S agalactiae
  • Gentamicin: Potential synergy when used with penicillin G for GBS

Penicillin, ampicillin, or vancomycin remains the treatment of choice for endocarditis.

If addition of an aminoglycoside to penicillin or ampicillin is under consideration to treat GBS infection, it is important to test for aminoglycoside sensitivity, because synergy is not observed if the organism is not sensitive to aminoglycosides. Keep in mind that group B streptococcal isolate can be resistant to one aminoglycoside and sensitive to another.

Surgery

Although medical therapy should cure many GBS infections, those involving skin, soft tissue, and bone may not be cured with antibiotics alone and may require surgical intervention, such as the following:

  • Surgical emergencies: Necrotizing fasciitis, septic arthritis, and epidural abscess
  • Empyema drainage in cases of pneumonia
  • Heart valve replacement in cases of endocarditis, bacteremia, and sepsis
  • Surgery plus parenteral antibiotics for soft-tissue infection, septic arthritis, osteomyelitis, discitis, and epidural abscess
  • Intervention for relief of GU obstruction in UTIs
  • Drainage for pelvic abscesses

See Treatment and Medication for more detail.

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Background

Group B Streptococcus, also known as Streptococcus agalactiae, was once considered a pathogen of only domestic animals, causing mastitis in cows. S agalactiae is now best known as a cause of postpartum infection and as the most common cause of neonatal sepsis. More recently, numerous series have described S agalactiae as a cause of infection in nonpregnant adults, providing descriptions of the clinical spectrum of disease, including clinical features, risk factors, therapy, and outcome of group B streptococcal infection in nonpregnant adults.

Group B streptococci colonize the vaginal and gastrointestinal tracts in healthy women, with carriage rates ranging from 15%-45%. Neonates can acquire the organism vertically in utero or during delivery from the maternal genital tract. Although the transmission rate from mothers colonized with S agalactiae to neonates delivered vaginally is approximately 50%, only 1-2% of colonized neonates go on to develop invasive group B streptococcal disease.[1]

Group B streptococcal neonatal sepsis is rare, but it is more common in the setting of prematurity and prolonged rupture of the membranes. Because of the ubiquity of S agalactiae colonization in women and the rarity of group B streptococcal neonatal sepsis, prevention of the disease is difficult. Many pregnant women require treatment to prevent a single neonatal infection. Immunoprophylaxis and chemoprophylaxis have both been studied as solutions to this problem.

Neonatal group B streptococcal disease is divided into early and late disease. Early group B streptococcal neonatal sepsis often presents within 24 hours of delivery but can become apparent up to 7 days postpartum. No specific clinical features differentiate early group B streptococcal disease from that caused by other pathogens. Pneumonia with bacteremia is common, while meningitis is less likely.

Late group B streptococcal neonatal sepsis is defined as infection that presents between one week postpartum and age 3 months. Late disease commonly involves group B Streptococcus serotype III, typically characterized by bacteremia and meningitis.

The absence of antibody to group B streptococci in infants is a risk factor for infection. Because antibodies to group B streptococci provide protection against disease in animal models, there is an ongoing interest in vaccination as an approach for reducing the incidence of group B streptococcal colonization in healthy women. Vaccine development was once promising, but shifting serotypes of group B streptococci responsible for clinical disease have limited this approach. Other factors that have made this approach less attractive include problems related to access to vaccination by women of childbearing age and the emotion and possible litigation associated with vaccination during pregnancy.

The current approach to the prevention of group B streptococcal infection in pregnancy approach requires intrapartum antimicrobial prophylaxis in term women with culture evidence of recent vaginal or rectal group B streptococcal infection. This has become a national standard owing to efforts by the Centers for Disease Control and Prevention (CDC) in 1995.[2] Women without a known group B streptococci status delivering before 37 weeks' gestation with premature rupture of the membranes or intrapartum fever are also candidates for intrapartum antimicrobial prophylaxis. Penicillin or ampicillin is the initial approach. Clindamycin and erythromycin are standard in individuals with penicillin allergy, but group B streptococci are no longer always sensitive to these two drugs.

Only in the last 3 decades has the role of group B streptococci as a serious pathogen in the nonpregnant adult been well defined. Numerous studies have allowed description of the clinical spectrum of disease, including clinical features, risk factors, therapy, and outcomes.

S agalactiae infection is extremely rare in healthy individuals and is almost always associated with underlying abnormalities. Among published series, diabetes mellitus and malignancy are consistently the most common underlying diseases associated with infection.[3] Other conditions associated with group B streptococcal infection in adults include cardiovascular and genitourinary abnormalities, neurologic deficits, cirrhosis, steroids, AIDS, renal dysfunction, and peripheral vascular disease. Relapse is not uncommon, with approximately 5% of nonpregnant adults eventually experiencing a second episode of group B streptococcal disease.[4]

Group B streptococcal infection in elderly people (≥70 y) is strongly linked to congestive heart failure and being bedridden, with urinary tract infection, pneumonia, and soft-tissue infection as the most common manifestations of infection. Neurologic illness is associated with pneumonia in elderly people, possibly due to aspiration of group B streptococci from the upper respiratory tract. Nosocomial group B streptococcal infection was common in this group and is described in other series. The source of this infection is not always clear, but the genitourinary tract and skin are thought to be the sources of some nosocomial infections.

Group B streptococci are found commonly in the gastrointestinal tract and have been found to colonize the urethra in both men and women without causing infection. Group B streptococci can also colonize the upper respiratory tract. Colonization also is observed in wound and soft tissue cultures in the absence of obvious infection. Determining the acquisition and transmission of S agalactiae can be puzzling, as it is very invasive but produces little inflammation at the entry site.

Primary group B streptococcal bacteremia without an obvious source is a common presentation in adults. While one series suggests that group B streptococcal bacteremia is low-grade and easily controlled with little morbidity, other authors suggest that the clinical presentation may be that of classic sepsis with shock and may carry a high mortality. Sustained bacteremia may indicate endocarditis or an infected catheter. Group B streptococci can cause acute destructive endocarditis, which may require emergency valve replacement.

Urinary tract infections are a common manifestation of group B streptococcal disease and are observed in both pregnant and nonpregnant adults. Other presentations of group B streptococcal infection include pneumonia, skin and soft-tissue infections, septic arthritis, osteomyelitis, meningitis, peritonitis, and endo-ophthalmitis.

Group B Streptococcus remains sensitive to penicillin and ampicillin and was once also sensitive to cefazolin, erythromycin, and clindamycin. Although penicillin is the treatment of choice, it is unclear whether penicillin therapy provides a better outcome than other antibiotics.

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Pathophysiology

S agalactiae is a gram-positive coccus that, when cultured on sheep blood agar, forms glistening gray-white colonies with a narrow zone of beta hemolysis. It is an invasive encapsulated organism capable of producing severe disease in immunocompromised hosts. Group B streptococcal infection in the absence of associated comorbid medical conditions is rare.

The virulence is of S agalactiae is related to the polysaccharide toxin it produces. Immunity is mediated by antibodies to the capsular polysaccharide and is serotype-specific. Several serotypes are known—Ia, Ib, Ic, II, III, IV, V, VI, VII, and VIII.

Group B streptococci colonize the vagina, gastrointestinal tract, and the upper respiratory tract of healthy humans. The portal of entry is not apparent, but possible areas include the skin, genital tract, urinary tract, and respiratory tract.

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Epidemiology

Frequency

United States

Group B streptococcal neonatal sepsis occurs in 1.8-3.2 per 1000 live births. In 2005, early group B streptococcal neonatal sepsis was observed in 0.35 per 1000 births, while late sepsis was observed in 0.33 per 1000 births.[5] The incidence of early disease has decreased over the past decade, likely because of the CDC guidelines for the prevention of neonatal colonization with group B streptococci.

While the incidence of group B streptococcal disease in neonates appears to be decreasing, the rate in nonpregnant adults appears to be increasing, with an overall increase of 32% between 1999 and 2005.[5] A recently published study of surveillance data from 10 states found that the incidence of group B streptococcal infection in persons aged 15-64 years increased from 3.4 per 100,000 population in 1999 to 5 per 100,000 in 2005. In adults aged 65 years and older, the incidence increased from 21.5 per 100,000 population in 1999 to 26 per 100,000 in 2005.[5]

International

The role of group B streptococci in the developing world is not well defined. Carriage rates and serotypes in women in underdeveloped countries are similar to those observed in the industrial world. However, for unknown reasons, early group B streptococcal disease in infants is not documented in less-developed countries.

Mortality/Morbidity

Group B streptococcal disease results in significant mortality in both neonates and adults. While the mortality rate ranges from 9-47% in published reports, most studies find it to be approximately 20%.[4] The mortality rate is highest in elderly patients with comorbid medical conditions, and the manifestations most likely to result in death include endocarditis, meningitis, and pneumonia. The high mortality rate in elderly people with group B streptococcal infection may not reflect the organism itself but the predisposing condition or conditions that put the individual at risk for group B streptococcal infection.

The mortality rate of neonatal group B streptococcal infection is much less than that in nonpregnant adults. An increasing awareness of group B streptococcal infection in infants has led to improved outcomes in recent years.

Postpartum group B streptococcal infection is associated with a low mortality rate because the group at risk is composed of healthy young or middle-aged women.

Race

Group B streptococcal infection is more common in African Americans than in whites and is much more common in older African Americans than in older whites. These differences are probably due to socioeconomic differences rather than race.

Sex

Young and middle-aged women who undergo obstetrical and gynecological manipulation are at an increased risk of group B streptococcal infection.

Among nonpregnant patients, group B streptococcal infection has no sexual predilection.

Age

The mean age for group B streptococcal infection is 64 years.

A bimodal distribution is well recognized. Young and middle-aged healthy women with group B streptococcal infection secondary to obstetrical or gynecological manipulation is one group, while the second group is elderly persons with group B streptococcal infection as a complication of preexisting illness.

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Contributor Information and Disclosures
Author

Christian J Woods, MD, FCCP Associate Program Director for Internal Medicine, Associate Program Director for Pulmonary/Critical Care, Associate MICU Director, Attending in Infectious Diseases/Pulmonary/Critical Care, MedStar Washington Hospital Center

Christian J Woods, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, Infectious Diseases Society of America

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Cubist Pharmaceuticals.

Coauthor(s)

Charles S Levy, MD Associate Professor, Department of Medicine, Section of Infectious Disease, George Washington University School of Medicine

Charles S Levy, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, Medical Society of the District of Columbia

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor Mohamad Ossiani, MD, to the development and writing of this article.

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