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Group B streptococcal infections in nonpregnant adults

Group B streptococcal infections in nonpregnant adults
Miriam Baron Barshak, MD
Lawrence C Madoff, MD
Section Editor:
Daniel J Sexton, MD
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Dec 2022. | This topic last updated: Oct 03, 2022.

INTRODUCTION — Group B Streptococcus (GBS; Streptococcus agalactiae) is a gram-positive coccus that frequently colonizes the human genital and gastrointestinal tracts and the upper respiratory tract in young infants [1,2]. It is an important cause of infection in three populations:

Neonates – GBS infection is acquired in utero or during passage through the vagina. The most common manifestations of neonatal disease are bacteremia without a focus, sepsis, pneumonia, and/or meningitis. (See "Group B streptococcal infection in neonates and young infants".)

Pregnant individuals – GBS is a frequent cause of urinary tract infection, chorioamnionitis, postpartum endometritis, and bacteremia in pregnant women. (See "Group B streptococcal infection in pregnant individuals".)

Nonpregnant adults – GBS is a cause of bacteremia without a focus, sepsis, soft tissue infections, and other focal infections in nonpregnant adults.

The microbiology and pathogenesis of GBS infection and the epidemiology, clinical manifestations, diagnosis, and treatment of GBS infections in nonpregnant adults will be reviewed here. Prevention strategies through chemoprophylaxis and vaccination are discussed separately. (See "Vaccines for the prevention of group B streptococcal disease".)

MICROBIOLOGY — Streptococcus agalactiae, the sole member of Lancefield group B, forms small 3 to 4 mm, grey-white colonies that have a narrow zone of beta hemolysis on blood agar [3-5]. The group B antigen is a cell wall-associated carbohydrate that distinguishes GBS from other streptococcal species [5].

GBS is identified in the clinical laboratory by its characteristic properties:

Narrow zone of beta hemolysis

Production of CAMP factor, a phospholipase that enhances the hemolysis caused by beta lysins of many Staphylococcus aureus strains

Hydrolysis of hippurate [3,6]

Lack of hydrolysis of bile esculin agar [3,6]

Commercial kits with antisera that recognize the group B antigen are used to confirm the identity of isolates. Molecular methods such as real-time polymerase chain reaction are also used for rapid identification of GBS and are available commercially [7]. Whole genome sequencing may facilitate determination of serotype and antimicrobial resistance [8].

PATHOGENESIS — GBS produces many extracellular substances, some of which have a role either in virulence or as protective antigens [3]. The best characterized are the capsular polysaccharides, which confer serotype specificity to GBS [9-11]. The 10 currently recognized capsular serotypes (Ia, Ib, II, III, IV, V, VI, VII, VIII, and IX) confer virulence to the organism, at least in part, by inhibiting the deposition of complement components on the surface of the organism in the absence of serotype-specific antibody. Antibodies to capsular polysaccharide confer protection against invasive disease, at least in neonates and young infants [12].

For a particular strain of serotype III GBS that has been strongly associated with neonatal meningitis after the first week of life, a surface-anchored protein called hypervirulent GBS adhesin (HvgA) is thought to mediate its hypervirulence [13]. Expression of HvgA promotes adherence to the intestinal epithelium and cells that form the blood-brain barrier.

The two-component CovR/S regulatory system controls numerous gene products that impact the virulence of GBS [14]. GBS strains lacking CovR/S, which acts as a hemolysin repressor, accelerate amniotic barrier failure and penetrate chorioamniotic membranes in a hemolysin-dependent manner [15]. Some hyperhemolytic clinical isolates from females in preterm labor are associated with CovR/S mutations. These isolates have been shown to allow ascending infection and fetal injury.

C proteins and other related surface proteins also are known to be involved in protective immunity and may have a role in virulence [16-19]. The alpha C protein has been shown to have a role in invasion by GBS into cultured cervical epithelial cells that is related to binding of host glycosaminoglycans [20]. The beta C protein, found in most serotype Ib GBS, binds specifically to human immunoglobulin (Ig)A [17], suggesting a role in virulence. Antibody to this protein is protective in animal models. Both C proteins have been used in experimental vaccines either alone or conjugated to capsular polysaccharides [21].

Pilins, long known for their role in virulence of gram-negative pathogens, have also been demonstrated to occur in group B streptococci and function as adhesins, promote central nervous system entry, and enhance biofilm formation [22].

Multiple complete genomic sequences for GBS have been published and are available through online databases [23,24]. Complete genomic sequencing of 202 invasive GBS of serotype V belonging to a virulent multilocus sequence type (ST 1) revealed the presence of a novel alpha-like protein [25]. The genomic analysis also suggested that small genetic changes (often at loci encoding capsule biosynthesis proteins, pilus regulation, and 2-component regulators) drove phenotypic diversity and that recombination appeared relatively unimportant. Analysis of genomic data should enable the identification of new vaccine antigens and improve the understanding of pathogenic mechanisms and epidemiology of GBS.


Incidence — Despite sporadic reports of GBS infection in nonpregnant adults, it was not until intensive population-based surveillance was performed in the 1980s and 1990s that the emergence of this organism as an important pathogen in adults was appreciated. Incidence rates are particularly high in the United States and appear to be somewhat lower in Europe [26].

In the United States, the incidence of invasive GBS infection among the general population of nonpregnant adults was estimated at approximately 11 cases per 100,000 persons in 2016 [27]. This reflected an increased incidence since the 2008 estimate of 8 cases per 100,000, consistent with the previously noted trend of increasing incidence over time [28].

Furthermore, the incidence increases with age and has been reported to be as high as 26 per 100,000 in patients ≥65 years of age [1,28].

With the increased reported incidence among adults and the reductions in GBS infection in neonates and pregnant individuals, GBS infection in nonpregnant adults has been estimated to account for over three-fourths of invasive GBS disease in the United States and for 90 percent of the mortality [29].

Risk factors for the development of infection — Many groups have attempted to characterize the adult hosts most susceptible to invasive GBS infection. In most reports, the incidences among males and females have been comparable [1,30-32]; although in the United States, the incidence in males has more recently been increasing faster than in females [27]. Some studies have found a higher rate in African Americans than in White Americans [1,30-32].

Diabetes mellitus, particularly with poor glycemic control, and obesity have emerged as the most common underlying conditions in patients with invasive GBS infection [27,33]. Malignancy, human immunodeficiency virus (HIV) infection, and advanced hepatic and renal disease have been identified as risk factors in population-based studies [1,30,32,34]. Some studies have also reported higher rates of GBS infection in patients with alcoholism, cardiovascular disease, collagen vascular disease (with or without steroid use), and trauma [35]. The risk is markedly increased in older adults, particularly nursing home residents [1,36].

A case control study compared patients with invasive GBS infections to patients hospitalized for other illnesses [34]. On multivariate analysis, the odds ratios (OR) were highest for the following independent risk factors: cirrhosis (OR 9.7), diabetes mellitus (OR 3.0), stroke (OR 3.5), breast cancer (OR 4.0), decubitus ulcer (OR 4.0), and neurogenic bladder (OR 4.6). Nosocomial infection, which accounted for 22 percent of these cases, was associated strongly with central venous line placement (OR 30.9), and less strongly with diabetes, congestive heart failure, and seizure disorder.

An outbreak of GBS (serotype III, sequence type 238) bacteremia was reported in Singapore beginning in 2015, infection was associated with consumption of a Chinese-style, raw freshwater fish dish, yusheng [37]. GBS isolates of the same sequence type were identified in the freshwater fish food chain [38]. This indicates that, at least in some adult cases, bacteremia may occur following consumption of food containing GBS.

Carriage of the organism — There is no obvious immunodeficiency common to patients with the above underlying conditions. Some of these illnesses may simply predispose to bacterial invasion because of a loss of barrier protection in a chronically colonized site. GBS has been isolated from cultures of the human rectum, vagina, cervix, urethra, skin, and pharynx.

Females of childbearing age have been most intensively studied for GBS colonization; vaginal and rectal cultures are positive for the organism in 5 to 40 percent of these individuals [39]. The carriage rate increases with parity, is inversely correlated with age, and is lower in Mexican Americans than in African Americans or White Americans [40,41].

The rate of colonization in healthy young males and females was evaluated in a report of 462 college students living in a dormitory [42]. GBS colonization at one or more site (urine, vagina, anal orifice, throat) was present in 34 percent of the females and 20 percent of the males. The colonization rate was twice as high in sexually experienced compared with inexperienced students, suggesting that GBS may be transmitted by sexual contact. GBS colonization appears to be dynamic over time. In a study of 66 females who underwent recto-vaginal swab sampling for GBS every two weeks for a 12-week period, nearly 30 percent of females who were GBS-negative during initial screening became positive and 84 percent of those who screened positive initially became negative during the study period, despite stable levels of anticapsular antibodies [43].

GBS colonization rates have been reported in a number of other groups:

Nursing home residents and staff – Positive rectal cultures for GBS in 12 and 15 percent, respectively [44].

Men who have sex with men – Rectal GBS carriage in 25 percent [45].

A possibly lower carriage rate in individuals with diabetes [46], even though the incidence of invasive infection is substantially increased [1,34].

Serotyping of invasive strains — Some efforts have been made to identify the strains of GBS involved in infections in nonpregnant adults. GBS are classified into serotypes based upon structural differences in capsular polysaccharides (Ia, Ib, and II-IX) and the presence or absence of surface protein antigens [47].

One report comparing the serotype frequency in infants and adults found a predominance of serotype III and serotype Ia, with fewer isolates of serotypes II and V in infant infections. By contrast, the major isolate in adults was serotype V, accounting for 29 percent of the organisms; there were smaller numbers of isolates of serotypes Ia/c, Ib/c, and III [48].

Other reports confirm the predominance of serotype V in adult invasive GBS infections and suggest an increasing prevalence of this serotype in perinatal GBS infections as well [31,49]. Serotypes of GBS colonizing pregnant females have been found to differ in Japanese females, with a high proportion colonized with types VI and VIII, two serotypes rarely found in the United States [50]. Emergence of type VIII has been described in Denmark as well [51]. Serotypes of GBS causing adult infection also probably differ in diverse geographic regions.

SYNDROMES AND SITES OF CLINICAL INFECTIONS — A broad spectrum of adult GBS infections has been documented in the literature, both in hospital-based case reports and case series and in population-based surveys. Of these infections, 20 to 70 percent are nosocomial [34,52].

Skin and soft tissue — Skin and soft tissue infections account for 15 to 40 percent of all bacteremic episodes in population-based surveys [30,32]. Included in this group are foot ulcers, decubitus ulcers, cellulitis, abscesses, necrotizing fasciitis, balanitis, and sternal wound infections after coronary artery bypass grafting [53-55]. Several cases of necrotizing fasciitis associated with a toxic shock-like syndrome have been reported [55-57].

Cellulitis is the most frequent clinical manifestation of GBS-associated skin and soft tissue infections. Conditions such as lymphedema, vascular insufficiency, chronic dermatitis, or radiation-induced cutaneous injury are frequent predisposing factors [58]. Postcoital GBS-associated sepsis and thigh cellulitis following sexual intercourse has been described in females with vaginal GBS colonization and predisposing factors. (See "Cellulitis following pelvic lymph node dissection", section on 'Streptococcal sex syndrome'.)

Bacteremia without clear source — Primary bacteremias comprise 30 to 40 percent of invasive GBS episodes in population-based surveys and are fatal in 20 to 60 percent of cases [30,32]. In some reports, most of these infections are nosocomial [52,59]. One group found a mean of 16.5 days elapsed between admission and evidence of infection; 81 percent of deaths occurred less than 48 hours after the first blood culture isolate of GBS, despite appropriate treatment [59]. Another study also reported high mortality in inpatients with nosocomial GBS infections but found that most of the deaths were attributable to the underlying disease, which prompted the admission, and to a prolonged hospitalization [52].

Urinary tract — The urinary tract is the source of 5 to 15 percent of invasive GBS isolates in population-based studies [30,32]. Most of these infections occur in older adults [60]. Genitourinary infections include most commonly cystitis and pyelonephritis, but epididymitis, urethritis, and prostatitis have been reported as well [61,62].

In nonpregnant adults, the GBS colony count definition for urinary tract infection is the same as the standard definition of a positive urine culture (≥105 colony-forming units/mL). (See "Sampling and evaluation of voided urine in the diagnosis of urinary tract infection in adults".)

Patients with urinary tract symptoms, pyuria, and urine culture positive for GBS should receive antimicrobial therapy as outlined below. (See 'Treatment' below.)

Lower respiratory tract — Pneumonia accounts for 6 to 12 percent of invasive GBS episodes in population-based reports [30,32]. However, most of these infections are polymicrobial; GBS is most frequently isolated along with Staphylococcus aureus. A large number of these pneumonias are nosocomial, occur in older adults, and have case fatality rates in excess of 40 percent [34,52].

Occasionally, GBS is isolated in throat cultures of patients with pharyngitis. In most cases, this is likely to be GBS colonization rather than infection.

Bone and joint — Two to 15 percent of population-based invasive GBS cases involve bone and joint infections [30,32]. The majority of these infections are osteomyelitis and septic arthritis. Most are community-acquired and develop in large joints, which were already abnormal from prior arthritis, traumatic injury, or joint replacement surgery [60].

In a retrospective review of patients with septic arthritis in Thailand from 1990 to 2010, GBS was an emerging cause of septic arthritis in the later years of the study [63]. Among the 38 cases of GBS septic arthritis identified, 71 percent presented with concurrent cellulitis and more than 70 percent involved more than one joint, with mean involvement of 3.34 joints.

Endocarditis — Two to 9 percent of isolates of GBS from patients with invasive disease have endocarditis, according to population-based studies [30,32]. Endocarditis mainly occurs on native valves, involving the left-sided valves more commonly than the right sided, and is often associated with large, friable vegetations. The typical host in the preantibiotic era was a young woman with rheumatic heart disease in the period postpartum or postabortion. However, the most frequent patient with GBS endocarditis currently is over 50 years old. Young postpartum females constitute a large proportion of patients who develop GBS bacteremia, but this group does not commonly develop endocarditis in the absence of pre-existing valvular heart disease.

Mortality from GBS endocarditis, whether it presents as an acute or subacute infection, may reach 40 percent, suggesting that GBS valve infections are more virulent than those caused by most other streptococcal species [64]. In one study, the mortality rate for prosthetic valve endocarditis was 100 percent [65]. These mortality rates are similar to those associated with staphylococcal endocarditis. Some groups believe that early surgery should be considered, as there is some suggestion that combined medical-surgical therapy yields better outcomes [66]. Pericarditis with GBS has also been reported [67]. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Overview of management of infective endocarditis in adults".)

Meningitis — Approximately 4 percent of invasive GBS infections involve the central nervous system (CNS) in population-based surveys; GBS infections account for approximately 1 percent of all cases of meningitis [30,32]. GBS meningitis has been described following elective abortion [68]. An increase in adult GBS meningitis has been noted recently in Southeast Asia [69]; reasons for this trend are unclear.

GBS infection of the CNS occurs equally among immunocompromised and immunocompetent hosts, with a mortality of approximately 27 percent. Among older adults (≥65 years) the case fatality rate is as high as 56 percent [70]. The incidence of infection has a bimodal distribution, with peaks in patients in their mid-20s and another in their mid-60s. A large percentage of these patients present with fever, meningismus, neurologic deficits, and spinal fluid glucose, protein, and cell counts suggestive of bacterial meningitis [39]. (See "Clinical features and diagnosis of acute bacterial meningitis in adults".)

Other sites — GBS has been reported as a rare cause of hematogenously seeded endophthalmitis and is associated with poor visual prognosis despite aggressive therapy [71]. In addition, the organism has been isolated from peritoneal fluid. The organism is also rarely the etiologic agent in endocarditis and has been recovered from infected pacemakers, abdominal abscesses, mycotic aneurysms, the sinuses, the supraglottis, and the biliary tree [34,65,72-77].

Toxic shock-like syndrome — Several authors have described patients with a syndrome characterized by fever, rash, hypotension, and electrolyte imbalances in conjunction with urinary tract infections and necrotizing fasciitis caused by GBS [55-57,78,79]. One study described 19 patients with a toxic shock-like syndrome associated with GBS infection in Japan between 2009 and 2013 [80]. The syndrome was defined by the presence of septic shock, multiorgan failure, and GBS isolation from a normally sterile site. All of the patients were adults and many had underlying comorbidities. The mortality rate was >50 percent. Only 3 of the 19 developed rash. These patients had GBS isolates with serotypes and susceptibility patterns that were similar to each other but distinct from isolates of infants and vaginal swabs from females with invasive disease. It was posited that special virulence factors in these isolates could lead to a toxic shock-like syndrome, but the isolates were not tested for toxin production.

One group had previously reported the isolation of a "pyrogenic toxin" from the supernatant of GBS cultures from strains associated with a toxic shock-like syndrome [78]. Rabbits injected subcutaneously with this toxin developed a toxic shock-like picture and died. While these laboratory results were felt to indicate potential toxin production among a subset of GBS strains, no subsequent work has been published evaluating this.

DIAGNOSIS — Isolation of GBS from a normally sterile body site (eg, blood, cerebrospinal fluid [CSF], pleural fluid, and bone) confirms the diagnosis of GBS infection. GBS antigen may be detected in CSF, which occasionally may assist in the diagnosis of infection. However, antigen testing of other body fluids is not recommended.

Most GBS infections in adults have no distinctive features that would lead the clinician to suspect that this pathogen would be isolated. Risk factors in the host are usually appreciated after the organism has been recovered in cultures. (See 'Risk factors for the development of infection' above.)


Antimicrobial susceptibilities — GBS isolates have traditionally been uniformly penicillin sensitive, and penicillin G is the most active agent in vitro. GBS isolates are also usually susceptible to ampicillin, extended-spectrum penicillins, and first-, second-, and third-generation cephalosporins. Alternative agents with reliable activity against GBS include vancomycin, linezolid, and daptomycin. There are low rates of quinolone resistance.

There is a significant and rising resistance among GBS isolates to macrolides, tetracyclines, and clindamycin [73]. Approximately 7 to 55 percent of isolates are resistant to erythromycin, and 3 to 43 percent to clindamycin [27,81-86]. An increase in macrolide resistance among isolates of serotype V has been reported [87]. Documented fluoroquinolone resistance has been relatively uncommon [88,89], but appears to be increasing in some locations, including China [90], Taiwan [91], Japan [86,92], and Argentina [93].

Although rare, GBS isolates with reduced susceptibly to penicillin (PRGBS) have been identified, in particular in Hong Kong and Japan [92,94,95]. In one study from Japan, the rate of PRGBS increased from 2.3 percent between 2005 and 2006 to 14.7 percent between 2012 and 2013 [92]. Certain clinical features may be associated with higher likelihood of infection with PRGBS [86]; however, data are limited and further study is needed. Among PRGBS, most were also resistant/nonsusceptible to both macrolides and fluoroquinolones; as an example, fluoroquinolone resistance were reported in 37.7 percent of PRGBS in China and 95.6 percent of PRGBS in Japan [90,92]. Some studies have reported that PRGBS retain susceptibility to cephalosporins and vancomycin [86,92,94]. In a subsequent study from Japan, however, 36 percent of PRGBS were also resistant to ceftriaxone [96].

Regimen selection

Severe and/or life-threatening infections — Severe and/or life-threatening GBS infections (eg, bacteremia, endocarditis, septic arthritis, meningitis, osteomyelitis) are typically treated with intravenous (IV) antibiotics. High-dose penicillin G (3 to 4 million units IV every four hours), with its narrow spectrum and low toxicity, has long been the drug of choice for serious group B streptococcal infections. Because of convenience of dosing, many clinicians now use ceftriaxone, which is an acceptable first-line alternative, and there have been no reports of treatment failure.

For patients who are allergic to penicillins, a third generation cephalosporin (eg, ceftriaxone) or vancomycin are alternative treatment options depending on the severity of the penicillin allergy.

For patients with mild, non-immunoglobulin (Ig)E-mediated reactions to penicillin (eg, maculopapular rash beginning days into therapy), we generally select ceftriaxone, a cephalosporin with a side chain that is dissimilar to penicillin.

For patients with a suspected IgE mediated reaction to penicillin (eg, urticaria, anaphylaxis), ceftriaxone can be given by a test dose procedure. (See "Choice of antibiotics in penicillin-allergic hospitalized patients", section on 'Test dose procedure (graded challenge)'.)

For patients who cannot use a cephalosporin (eg, serious delayed reactions to beta-lactams), vancomycin is an alternative, although cases of vancomycin-resistant infections have been very rarely reported [97].

The treatment of the individual syndromes, including dosing and duration of treatment, are discussed separately:

Endocarditis. (See "Antimicrobial therapy of left-sided native valve endocarditis", section on 'Streptococcal groups A, B, C, F, and G' and "Antimicrobial therapy of prosthetic valve endocarditis", section on 'Streptococci'.)

Septic arthritis. (See "Septic arthritis in adults", section on 'Antibiotic therapy'.)

Meningitis. (See "Treatment of bacterial meningitis caused by specific pathogens in adults".)

Osteomyelitis. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Streptococci and enterococci' and "Nonvertebral osteomyelitis in adults: Treatment", section on 'Clinical approach'.)

Necrotizing fasciitis. (See "Necrotizing soft tissue infections".)

Toxic shock-like syndrome – Toxic shock-like syndrome due to GBS is rare. The addition of clindamycin to a beta-lactam is supported by analogy to group A streptococcal toxic shock syndrome and by a case report [79]. (See "Invasive group A streptococcal infection and toxic shock syndrome: Treatment and prevention".)

Pneumonia – Pneumonia is an uncommon manifestation of invasive GBS, and in such cases, most of the infections are polymicrobial and nosocomial. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Duration'.)

Uncomplicated bacteremia – For patients with uncomplicated bacteremia (ie, without metastatic infection, meningitis, osteomyelitis, endocarditis, or prosthetic material associated with risk for seeding during bacteremia), we generally suggest 14 days of intravenous therapy. However, the decision regarding duration of treatment for an individual patient may be affected by time to clearance of bacteremia and improvement in the signs of infection; a shorter course (eg, 10 days) may be appropriate in patients with rapid clearance of bacteremia and clinical improvement.

Mild to moderate infection — Certain non-life-threatening infections such as uncomplicated skin and soft tissue infections or simple cystitis can be treated with oral antibiotics at initial presentation. Oral antibiotics are also appropriate for some more severe infections (eg, pneumonia) following clinical response to initial parenteral therapy. Penicillins and cephalosporins are the treatment of choice.

Skin and soft tissue infection – Most cases of cellulitis are treated empirically to include coverage for S. aureus and streptococci, including GBS (see "Acute cellulitis and erysipelas in adults: Treatment", section on 'Selecting an antibiotic regimen'). In the event that a mild skin and soft tissue infection is known to be caused by GBS (eg, based on cultures of blood or wound cultures), preferred treatment options are penicillin VK 500 mg orally every six hours, amoxicillin 500 mg orally every eight hours, or cephalexin 500 mg four times daily. For patients who cannot take penicillins or cephalosporins (eg, serious delayed reactions to beta-lactams), and for whom desensitization to penicillin is not possible, in vitro susceptibility data and limited clinical experience suggest quinolones (eg, levofloxacin 750 mg daily) or trimethoprim-sulfamethoxazole (one double-strength tablet two times daily) may be effective; neither of these antibiotics have been studied in GBS in controlled trials. If available, susceptibility testing should be performed to confirm that the infecting organism is sensitive to the antibiotic chosen. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Selecting an antibiotic regimen'.)

For patients with GBS skin and soft tissue infection, the duration of therapy will depend on response to therapy; treatment courses typically range from 5 to 10 days. Patients should have a repeat evaluation after 24 to 48 hours to verify clinical response.

Management of recurrent cellulitis is discussed elsewhere. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Recurrent infection'.)

Acute simple cystitis – For simple cystitis caused by GBS, amoxicillin (500 mg every eight hours) is usually the preferred agent. Cephalosporins (preferably cephalexin 500 mg twice daily or cefuroxime 250 mg twice daily; cefpodoxime 100 mg twice daily if earlier-generation cephalosporins cannot be given) are reasonable alternatives. Beta-lactams are typically administered for five to seven days for simple cystitis. (See "Acute simple cystitis in females", section on 'Management'.)

For patients who cannot take penicillins or cephalosporins (eg, serious delayed reactions to beta-lactams), nitrofurantoin (100 mg orally twice daily for five days) is an alternative. (See "Acute simple cystitis in females", section on 'Alternative antimicrobial options'.)


Risk of recurrence — Recurrent GBS infection can occur. In one study of 395 nonpregnant adults with GBS infection who survived the initial infection and were followed for at least one year, 17 (4 percent) developed a second infection [98]. The median age of the patients with recurrent infection was 60 years and all had an underlying disease (systemic lupus erythematosus, cirrhosis, malignancy, diabetes mellitus, renal insufficiency, chronic obstructive pulmonary disease, renal transplant, neurologic disease, and lymphedema). The mean interval between infections was significantly shorter for the 13 patients (72 percent) with the same strain by molecular genetic analysis than for those who had a different strain (14 versus 43 weeks). Relapsed or recurrent infection could have arisen from ongoing gastrointestinal or genitourinary carriage, reinfection from a contact, or an inadequate course of treatment for the initial infection.

A subsequent study of nonpregnant adult patients in Taiwan, reported a 9.3 percent recurrence rate, with the urinary tract as the most common site of recurrence and serotype V as the most common serotype associated with recurrence [99]. Relapse was more common than reinfection, and the affected patients had high levels of comorbidity.

Mortality — Overall fatality rate associated with invasive GBS infection in nonpregnant adults varies in different reports.

In the United States, the estimated case fatality rate averaged 6.5 percent between 2008 and 2016, based on data from a national surveillance network [27]. Earlier studies had reported mortality rates of 15 to 38 percent among nonpregnant adults in the United States [1,30,47,59].

Reports from other countries have also varied [100,101]. As an example, in a retrospective study of 224 patients with invasive GBS infection seen between 2013 and 2017 at a large tertiary care hospital in Thailand, the 30-day mortality rate was 11 percent [100]. Among the 76 percent who had bacteremia, the mortality rate was higher (14 versus 2 percent in those without bacteremia); pneumonia was also associated with higher mortality.

Factors associated with worse outcome have included: age over 65 years, central nervous system disease, alcohol use disorder, shock, kidney injury and disease, impaired level of consciousness, and confinement to bed [31,41,102]. Cirrhosis and more advanced Child-Pugh class have also associated with significantly higher mortality rates with GBS bacteremia [103].


Microbiology and pathogenesisStreptococcus agalactiae forms small 3 to 4 mm, grey-white colonies that have a narrow zone of beta hemolysis on blood agar and is the sole member of Lancefield group B. Virulence factors include capsular polysaccharides and other proteins that confer hypervirulence, protection against host’s immune system, and ability to adhere to cells and form biofilm. (See 'Microbiology' above and 'Pathogenesis' above.)

Epidemiology − Group B Streptococcus (GBS; Streptococcus agalactiae) is an increasingly recognized cause of bacteremia without a focus, sepsis, soft tissue infections, and other focal infections in nonpregnant adults. Patients with advanced age or underlying chronic diseases including diabetes, cancer, and renal/liver dysfunction are particularly susceptible, and these infections are associated with high morbidity and mortality despite treatment with appropriate antibiotics. (See 'Introduction' above and 'Epidemiology' above.)

Sites of clinical infection

GBS bacteremia frequently occurs without a clear source. In such cases, the infection may be nosocomial and is associated with high mortality rates.

Cellulitis is the most frequent clinical manifestation of GBS-associated skin and soft tissue infections, often in the setting of lymphedema, vascular insufficiency, or chronic dermatitis. Cases of necrotizing fasciitis with a toxic shock-like syndrome have also been reported. (See 'Skin and soft tissue' above.)

Genitourinary infections most commonly include cystitis and pyelonephritis, in addition to epididymitis, urethritis, and prostatitis. (See 'Urinary tract' above.)

GBS pulmonary infections are typically polymicrobial, most frequently with Staphylococcus aureus. (See 'Lower respiratory tract' above.)

GBS osteomyelitis and septic arthritis are generally community-acquired and affect large joints. (See 'Bone and joint' above.)

Other less common GBS infections include endocarditis, meningitis, endophthalmitis, intra-abdominal infections, and mycotic aneurysms. (See 'Syndromes and sites of clinical infections' above.)

Diagnosis − Isolation of GBS from a normally sterile body site (eg, blood, cerebrospinal fluid, pleural fluid, and bone) confirms the diagnosis of GBS infection (see 'Diagnosis' above). GBS can colonize the rectum, vagina, cervix, urethra, skin, and pharynx.


Severe and/or life-threatening infections − Severe and/or life-threatening GBS infections (eg, bacteremia, endocarditis, septic arthritis, meningitis, osteomyelitis) are typically treated with intravenous (IV) antibiotics. High-dose penicillin G (3 to 4 million units IV every four hours), with its narrow spectrum and low toxicity, has long been the drug of choice for serious group B streptococcal infections. Because of convenience of dosing, many clinicians now use ceftriaxone, which is an acceptable first-line alternative, and there have been no reports of treatment failure. Vancomycin is an alternative treatment option for patients with severe beta-lactam allergies. (See 'Severe and/or life-threatening infections' above.)

Mild to moderate infection − Certain non-life-threatening infections such as uncomplicated skin and soft tissue infections or simple cystitis can be treated with oral antibiotics at initial presentation. Oral antibiotics are also appropriate for some more severe infections (eg, pneumonia) following clinical response to initial parenteral therapy. Penicillins and cephalosporins are the treatment of choice. (See 'Mild to moderate infection' above.)

Antimicrobial susceptibility − GBS resistance to macrolides, tetracyclines, and clindamycin is rising worldwide, and resistance to cephalosporins is increasing in Asia. (See 'Antimicrobial susceptibilities' above.)

Duration − The duration of therapy depends on the type of infection being treated. (See 'Severe and/or life-threatening infections' above and 'Mild to moderate infection' above.)

Outcomes − High mortality rates have been reported for GBS infections that occur outside the peripartum period. Relapsed and recurrent infections also occasionally occur, possibly from ongoing gastrointestinal or genitourinary carriage, reinfection from a contact, or an inadequate course of treatment for the initial infection. (See 'Outcome of infection' above.)

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