Group B Streptococcus (GBS) Infections

Updated: Apr 21, 2021
  • Author: Christian J Woods, MD, FACP, FCCP, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
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Practice Essentials

Group B streptococcus (GBS), also known as Streptococcus agalactiae, is recognized as a leading cause of postpartum infection and neonatal sepsis. Infection in healthy, nonpregnant adults is becoming more common, especially among young to middle-aged women with diabetes.

GBS organisms colonize the vagina, gastrointestinal tract, and the upper respiratory tract in healthy humans. In the frail elderly, GBS infection is strongly linked with congestive heart failure.

Signs and symptoms of GBS infection include the following:

·    GBS pneumonia is infrequently encountered. It is primarily seen in older adults with diabetes or with a variety of neurologic deficits; its presentation is the same as that of any bacterial pneumonia (fever, shortness of breath, chest pain, pleuritic pain, cough).

·    GBS meningitis is usually restricted to neonates. In adults, GBS meningitis is associated with a variety of anatomic abnormalities that are complications of neurosurgery. Common manifestations include fever, headache, nuchal rigidity, and confusion.

·     In patients with GBS bacteremia, the source of the bloodstream infection cannot usually  be identified. Clinical manifestations include fever, malaise, confusion, chest pain, shortness of breath, myalgia, and arthralgia.

·    Skin and soft-tissue infection, decubitus ulcers, and colonization of foot infections in patients with diabetes can also result from GBS infection. Clinical manifestations include fever, malaise, localized pain, and cellulitis.

·    Osteomyelitis, arthritis, and diskitis may also occur; common manifestations include fever, malaise, localized pain, cellulitis, arthralgia, arthritis, and weakness.

·    Chorioamnionitis, endometritis, and urinary tract infections (ranging from asymptomatic bacteriuria to cystitis and pyelonephritis with bacteremia) can cause fever, dysuria, flank pain, and pelvic pain.


Examination of patients with GBS infection may reveal 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

Laboratory tests

Laboratory tests performed for a patient with suspected GBS infection may include the following:

·    Gram stain

·    Isolation of GBS from blood, cerebrospinal fluid, and/or a site of local suppuration: the only method for diagnosing invasive GBS infection

·    GBS antigen detection in blood, cerebrospinal fluid, and/or urine

Imaging tests

The following imaging studies may be performed for a patient suspected of having GBS infection:

·    Chest radiography: May show pneumonia in elderly bedridden patient with fever, neurologic deficits, or other relevant symptoms; infiltrate or effusion may be seen

·    Radiography of an affected region in a patient with diabetes or one who is elderly or bedridden with fever and relevant symptoms: May reveal evidence of gas or bone destruction in such patients with soft-tissue infection, osteomyelitis, diskitis, epidural abscess, wound infection, necrotizing fasciitis, decubitus ulcer

·    Computed tomography (CT) scanning of an affected region: May reveal phlegmon, abscess, or osteomyelitis

·    CT scanning of the head in a patient who has undergone a neurosurgical procedure with fever and other relevant symptoms: May show meningitis; may reveal an abscess or contiguous infection

·    Echocardiography in a patient with fever of unclear origin: May demonstrate vegetations or evidence of valve destruction

·    Ultrasonography of the genitourinary  tract or pelvis in a postpartum woman or older man or woman with fever and relevant symptoms: May reveal evidence of genitourinary obstruction or abscess

·    CT scanning and magnetic resonance imaging (MRI) of the genitourinary system or pelvis: May show evidence of obstruction or abscess


The following are procedures that may be performed when GBS infection is suspected:

·    Lumbar puncture for suspected GBS meningitis: First, rule out increased intracranial pressure with CT scanning, then perform lumbar puncture.

·    Diagnostic and therapeutic thoracentesis for suspected GBS pneumonia: in the presence of pleural effusion; empyema requires drainage by thoracentesis, chest tube, or surgery

·    Valve replacement for GBS bacteremia, endocarditis, and line-related sepsis: Caused by destructive endocarditis

·    Diagnostic aspiration and curative surgery for GBS soft-tissue infection, arthritis, osteomyelitis, diskitis, and epidural abscess

·    Diagnostic aspiration/tap with ultrasonography or CT guidance for urinary tract infection or pelvic abscess to isolate the organism, relieve obstruction, or drain an abscess



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

·    Penicillin G: Drug of choice for GBS infection

·    Ampicillin: Another drug of choice for GBS infection

     Vancomycin: Initial treatment of choice for GBS infection in patients who are allergic to penicillin (owing to possible resistance to clindamycin)

      Penicillin, ampicillin, or vancomycin: Treatment of choice for endocarditis

·    Clindamycin: Sensitivity testing must be done because of increasing resistance; oral 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 or ceftriaxone: Alternative to penicillin for GBS infection; not effective for GBS meningitis

If none of the listed antibiotics can be used, a consultation with an infectious diseases specialist is strongly recommended.


Although medical therapy should resolve many GBS infections, those involving skin, soft tissue, and bone may not be resolved with antibiotics alone and may require surgical intervention, including the following infections:

·    Surgical emergencies: Necrotizing fasciitis, septic arthritis, and epidural abscess

·    Empyema drainage in cases of pneumonia

·    Heart valve replacement in patients with endocarditis, bacteremia, or sepsis

·    Surgery plus parenteral antibiotics for soft-tissue infection, septic arthritis, osteomyelitis, diskitis, and epidural abscess

·    Intervention for relief of genitourinary obstruction in patients with urinary tract infections

·    Drainage for pelvic abscesses



Group B streptococcus (GBS), also known as Streptococcus agalactiae, was once considered a pathogen of domestic animals only, 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 outcomes of GBS infection in nonpregnant adults.

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

GBS neonatal sepsis is rare, but it is more common in the setting of prematurity and prolonged rupture of the membranes. Rates of mortality and morbidity are increased in preterm newborns with early-onset GBS disease. [2]  Because of the ubiquity of S agalactiae colonization in women and the rarity of GBS 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 GBS disease is divided into early and late disease. Early GBS neonatal sepsis often presents within 24 hours of delivery but can become apparent up to 7 days afterward. No specific clinical features differentiate early GBS disease from infections caused by other pathogens. Pneumonia with bacteremia is common, whereas meningitis is less likely.

Late GBS neonatal sepsis is defined as infection that presents between 1 week post partum and the age of 3 months. Late disease commonly involves GBS serotype III, typically characterized by bacteremia and meningitis.

The absence of antibody to GBS in infants is a risk factor for infection. Because antibodies to GBS provide protection against disease in animal models, there is an ongoing interest in vaccination as an approach to reducing the incidence of GBS colonization in healthy women. Vaccine development was once promising; however, shifting serotypes of GBS 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 emotional responses and possible litigation associated with vaccination during pregnancy.

The current approach to the prevention of GBS infection during pregnancy requires intrapartum antimicrobial prophylaxis in women at term who have culture evidence of recent vaginal or rectal GBS infection. This has become the standard owing to the efforts of the American College of Obstetrics and Gynecology and the Centers for Disease Control and Prevention in 2010 and 2020. [3, 4]  Women without a known GBS status delivering before 37 weeks' gestation with premature rupture of the membranes or intrapartum fever are also candidates for intrapartum antimicrobial prophylaxis. Administration of penicillin or ampicillin is the initial approach. Clindamycin and erythromycin used to be the standard in individuals with penicillin allergy, but group B streptococci are no longer always sensitive to these 2 drugs. Because of increasing resistance to clindamycin and erythromycin, [5]  vancomycin is now the agent of choice for pregnant women with high-risk penicillin allergy. Clindamycin should only be used if testing for resistance to clindamycin has been performed on GBS isolated cultures. [3]

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

Streptococcus agalactiae infection is becoming more common in nonpregnant adults and is almost always associated with underlying abnormalities. In published series, diabetes mellitus, obesity, and malignancy have been consistently reported as the most common underlying diseases associated with infection. [6] Other conditions associated with GBS infection in adults include HIV, cirrhosis, advanced kidney disease, cardiovascular and genitourinary abnormalities, neurologic deficits, steroid therapy, and peripheral vascular disease. [7]  Relapse is not uncommon, with approximately 5% of nonpregnant adults eventually experiencing a second episode of GBS disease. [8]

GBS infection in elderly people (≥70 years) is strongly linked to congestive heart failure and being bedridden; urinary tract infection, pneumonia, and soft-tissue infection are the most common manifestations of infection. [9]  Neurologic disease is associated with pneumonia in elderly people, possibly resulting from aspiration of group B streptococci from the upper respiratory tract. Nosocomial GBS infection is 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 commonly found 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 is also observed in wound and soft tissue cultures in the absence of obvious infection. Determining the site of origin of acquisition and transmission of S agalactiae can be puzzling because these bacteria are very invasive but produce little inflammation at the point of entry.

Primary GBS bacteremia without an obvious source is a common presentation in adults. Although one study suggests that GBS bacteremia is a low-grade infection and easily controlled with little morbidity, results of other studies suggest that the clinical presentation may be the same as that of classic sepsis with shock and may carry a high mortality rate. 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 GBS disease and are observed in both pregnant and nonpregnant adults. Other presentations of GBS infection include pneumonia, skin and soft-tissue infections, septic arthritis, osteomyelitis, meningitis, peritonitis, and endo-ophthalmitis.

Group B streptococci remain sensitive to penicillin and ampicillin and were once also sensitive to cefazolin, erythromycin, and clindamycin. Although penicillin is the treatment of choice, it is unclear whether use of penicillin provides a better outcome than use of other antibiotics.



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

The virulence 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. In the United States, serotypes Ia, Ib, II, III, and V have been shown to be associated with invasive disease. [9]

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




United States

GBS neonatal sepsis occurs in 1.8 to 3.2 per 1000 live births. In 2005, early GBS neonatal sepsis was observed in 0.35 per 1000 births, whereas late sepsis was observed in 0.33 per 1000 births. [10] The incidence has decreased from 1.8 per 1000 births in the 1990s to 0.23 in 2015, likely because of the implementation of the American College of Obstetricians and Gynecologists and Centers for Disease Control and Prevention guidelines for antibiotic prophylaxis for pregnant women with colonization with group B streptococci. [11]

Although the incidence of GBS 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 and an incidence of 8 cases per 100,000 population. [10]  In studies, investigators have estimated that in 2016, the rate for nonpregnant adults in the general public was approximately 11 cases per 100,000 population. [12]


The role of group B streptococci in the developing world is not well defined. However, a meta-analysis of GBS disease in 53 countries, published in 2017, showed a pooled incidence of invasive GBS disease of 0.49 per 1000 live births. [13]  The meta-analysis also showed the incidence of early-onset GBS disease to be 0.41 per 1000 births and the incidence of late-onset GBS disease to be 0.26 per 1000 births. [13]  Carriage rates and serotypes in women in underdeveloped countries are similar to those observed in the industrial world.

Mortality and Morbidity

GBS disease results in significant mortality in both neonates and adults. Although the mortality rate ranges from 947% in published reports, most studies have revealed it to be approximately 20%. [8] The case fatality rate in the United States between 2008 and 2016 was found to be, on average, 6.5% for invasive GBS infection. [12]  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 GBS infection may not reflect the organism itself but the predisposing condition or conditions that put the individual at risk for GBS infection.

The mortality rate for neonatal GBS infection is much lower than that for GBS infection in nonpregnant adults. An increasing awareness of GBS infection in infants has led to improved outcomes in recent years.

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


GBS infection is more common in Black individuals than in White individuals and is much more common in older Black adults than in older White adults. These differences are probably due to socioeconomic factors rather than race. [12]


Young and middle-aged women who undergo obstetric and gynecologic manipulation have an increased risk for GBS infection.

Among nonpregnant patients, GBS infection has no sexual predilection. Incidence has been increasing in men compared with women in the United States. [12]


The mean age of adult patients with GBS infection is 64 years.

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