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Group B streptococcal infections in nonpregnant adults

Group B streptococcal infections in nonpregnant adults
Authors:
Miriam Baron Barshak, MD
Lawrence C Madoff, MD
Section Editor:
Daniel J Sexton, MD
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Sep 2021. | This topic last updated: Oct 26, 2021.

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

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

GBS infection in nonpregnant adults will be reviewed here. The microbiology of infections caused by this organism and prevention strategies through chemoprophylaxis and vaccination are discussed separately. (See "Group B Streptococcus: Virulence factors and pathogenic mechanisms" and "Early-onset neonatal group B streptococcal disease: Prevention" and "Vaccines for the prevention of group B streptococcal disease".)

EPIDEMIOLOGY

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 [3].

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 [4]. 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 [5].

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 [1,5].

With the increased reported incidence among adults and the reductions in GBS infection in neonates and pregnant women, 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 [6].

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 men and women have been comparable [1,7-9]; although in the United States, the incidence in men has more recently been increasing faster than in women [4]. Some studies have found a higher rate in African Americans than in Caucasians [1,7-9].

Diabetes mellitus, particularly with poor glycemic control, and obesity have emerged as the most common underlying conditions in patients with invasive GBS infection [4,10]. Malignancy, HIV infection, and advanced hepatic and renal disease have been identified as risk factors in population-based studies [1,7,9,11]. 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 [12]. The risk is markedly increased in older adults, particularly nursing home residents [1,13].

A case control study compared patients with invasive GBS infections to patients hospitalized for other illnesses [11]. 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 [14]. GBS isolates of the same sequence type were identified in the freshwater fish food chain [15]. 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.

Women 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 women [16]. The carriage rate increases with parity, is inversely correlated with age, and is lower in Mexican Americans than in African Americans or Caucasians [17,18].

The rate of colonization in healthy young men and women was evaluated in a report of 462 college students living in a dormitory [19]. GBS colonization at one or more site (urine, vagina, anal orifice, throat) was present in 34 percent of the women and 20 percent of the men. 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 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 [20].

Male homosexuals – rectal GBS carriage in 25 percent [21].

A possibly lower carriage rate in diabetics [22], even though the incidence of invasive infection is substantially increased [1,11].

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 [23]. (See "Group B Streptococcus: Virulence factors and pathogenic mechanisms".)

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 [24].

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 [8,25]. Serotypes of GBS colonizing pregnant women have been found to differ in Japanese women, with a high proportion colonized with types VI and VIII, two serotypes rarely found in the United States [26]. Emergence of type VIII has been described in Denmark as well [27]. 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 [11,28].

Skin and soft tissue — Skin and soft tissue infections account for 15 to 40 percent of all bacteremic episodes in population-based surveys [7,9]. Included in this group are foot ulcers, decubitus ulcers, cellulitis, abscesses, necrotizing fasciitis, balanitis, and sternal wound infections after coronary artery bypass grafting [29-31]. Several cases of necrotizing fasciitis associated with a toxic shock-like syndrome have been reported [31-33].

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 [34]. Postcoital GBS-associated sepsis and thigh cellulitis following sexual intercourse has been described in women 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 [7,9]. In some reports, most of these infections are nosocomial [28,35]. 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 [35]. 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 [28].

Urinary tract — The urinary tract is the source of 5 to 15 percent of invasive GBS isolates in population-based studies [7,9]. Most of these infections occur in elderly adults [36]. Genitourinary infections include most commonly cystitis and pyelonephritis, but epididymitis, urethritis, and prostatitis have been reported as well [37,38].

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 [7,9]. 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 [11,28].

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 [7,9]. 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 [36].

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 [39]. 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 [7,9]. 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 women 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 [40]. In one study, the mortality rate for prosthetic valve endocarditis was 100 percent [41]. 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 [42]. Pericarditis with GBS has also been reported [43]. (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 [7,9]. GBS meningitis has been described following elective abortion [44]. An increase in adult GBS meningitis has been noted recently in Southeast Asia [45]; 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 [46]. 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 [16]. (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 [47]. 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 [11,41,48-53].

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 [31-33,54,55]. One study described 19 patients with a toxic shock-like syndrome associated with GBS infection in Japan between 2009 and 2013 [56]. 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 women 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 [54]. 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.)

TREATMENT

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 [49]. Approximately 7 to 55 percent of isolates are resistant to erythromycin, and 3 to 43 percent to clindamycin [4,57-62]. An increase in macrolide resistance among isolates of serotype V has been reported [63]. Documented fluoroquinolone resistance has been relatively uncommon [64,65], but appears to be increasing in some locations, including China [66], Taiwan [67], Japan [62,68], and Argentina [69].

Although rare, GBS isolates with reduced susceptibly to penicillin (PRGBS) have been identified, in particular in Hong Kong and Japan [68,70,71]. 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 [68]. Certain clinical features may be associated with higher likelihood of infection with PRGBS [62]; 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 [66,68]. Some studies have reported that PRGBS retain susceptibility to cephalosporins and vancomycin [62,68,70]. In a subsequent study from Japan, however, 36 percent of PRGBS were also resistant to ceftriaxone [72].

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 [73].

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 [55]. (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 "Cellulitis and skin abscess in adults: Treatment"). 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 "Cellulitis and skin abscess in adults: Treatment", section on 'Clinical approach'.)

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 "Cellulitis and skin abscess 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 women", 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 women", section on 'Alternative antimicrobial options'.)

OUTCOME OF INFECTION

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 [74]. 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 [75]. 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 [4]. Earlier studies had reported mortality rates of 15 to 38 percent among nonpregnant adults in the United States [1,7,23,35].

Reports from other countries have also varied [76,77]. 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 [76]. 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 [8,18,78]. Cirrhosis and more advanced Child-Pugh class have also associated with significantly higher mortality rates with GBS bacteremia [79].

SUMMARY AND RECOMMENDATIONS

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.)

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.)

GBS bacteremia frequently occurs without a clear source. In such cases, the infection is usually nosocomial and is associated with high mortality rates. (See 'Bacteremia without clear source' above.)

Genitourinary infections most commonly include cystitis and pyelonephritis, in addition to epididymitis, urethritis, and prostatitis. GBS pulmonary infections are typically polymicrobial, most frequently with Staphylococcus aureus. GBS osteomyelitis and septic arthritis are generally community-acquired and affect large joints. Other less common GBS infections include endocarditis, meningitis, endophthalmitis, intra-abdominal infections, and mycotic aneurysms. (See 'Syndromes and sites of clinical infections' above.)

GBS can colonize the rectum, vagina, cervix, urethra, skin, and pharynx. 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.)

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.)

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.)

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

The duration of therapy depends on the type of infection being treated. (See 'Treatment' above.)

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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  41. Sambola A, Miro JM, Tornos MP, et al. Streptococcus agalactiae infective endocarditis: analysis of 30 cases and review of the literature, 1962-1998. Clin Infect Dis 2002; 34:1576.
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  43. Vartian CV, Septimus EJ. Tricuspid valve group B streptococcal endocarditis following elective abortion. Rev Infect Dis 1991; 13:997.
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  45. Wilder-Smith E, Chow KM, Kay R, et al. Group B streptococcal meningitis in adults: recent increase in Southeast Asia. Aust N Z J Med 2000; 30:462.
  46. Domingo P, Barquet N, Alvarez M, et al. Group B streptococcal meningitis in adults: report of twelve cases and review. Clin Infect Dis 1997; 25:1180.
  47. Lee SY, Chee SP. Group B Streptococcus endogenous endophthalmitis : case reports and review of the literature. Ophthalmology 2002; 109:1879.
  48. Bayer AS, Chow AW, Anthony BF, Guze LB. Serious infections in adults due to group B streptococci. Clinical and serotypic characterization. Am J Med 1976; 61:498.
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  53. Baddour LM, Cox JW Jr. Group B streptococcal infection of a pacemaker wire following sigmoidoscopy. Clin Infect Dis 1992; 15:1069.
  54. Schlievert PM, Gocke JE, Deringer JR. Group B streptococcal toxic shock-like syndrome: report of a case and purification of an associated pyrogenic toxin. Clin Infect Dis 1993; 17:26.
  55. Begley JS, Barnes RC. Group B streptococcus toxic shock-like syndrome in a healthy woman: a case report. J Reprod Med 2007; 52:323.
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Topic 3171 Version 35.0

References

1 : Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis.

2 : Group B streptococcal disease in the United States, 1990: report from a multistate active surveillance system.

3 : Changing epidemiology of group B streptococcal infections among adults in Iceland: 1975-2014.

4 : Epidemiology of Invasive Group B Streptococcal Infections Among Nonpregnant Adults in the United States, 2008-2016.

5 : Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005.

6 : Increasing burden of invasive group B streptococcal disease in nonpregnant adults, 1990-2007.

7 : A population-based assessment of invasive disease due to group B Streptococcus in nonpregnant adults.

8 : Invasive group B streptococcal disease: the emergence of serotype V.

9 : Invasive group B streptococcal disease in adults. A population-based study in metropolitan Atlanta.

10 : Risk Factors and Mortality Rates Associated With Invasive Group B Streptococcus Infections Among Patients in the US Veterans Health Administration.

11 : Risk factors for group B streptococcal disease in adults.

12 : Invasive group B streptococcal disease in nonpregnant adults.

13 : Invasive group B streptococcal disease in Maryland nursing home residents.

14 : Group B Streptococcus Serotype III Sequence Type 283 Bacteremia Associated with Consumption of Raw Fish, Singapore.

15 : Group B Streptococcus Infections Caused by Improper Sourcing and Handling of Fish for Raw Consumption, Singapore, 2015-2016.

16 : Group B streptococcal meningitis in adults.

17 : Population-based risk factors for neonatal group B streptococcal disease: results of a cohort study in metropolitan Atlanta.

18 : Epidemiology of group B streptococcal disease. Risk factors, prevention strategies, and vaccine development.

19 : Prevalence of group B streptococcus colonization and potential for transmission by casual contact in healthy young men and women.

20 : Rectal colonization by group B beta-hemolytic streptococci in a geriatric population.

21 : Group B streptococci--gastrointestinal organisms?

22 : Comparison of carriage rates of group B streptococcus in diabetic and nondiabetic persons.

23 : The changing spectrum of group B streptococcal disease.

24 : Serotype IX, a Proposed New Streptococcus agalactiae Serotype.

25 : Invasive disease due to group B Streptococcus in pregnant women and neonates from diverse population groups.

26 : Serotypes VI and VIII predominate among group B streptococci isolated from pregnant Japanese women.

27 : Emergence of invasive serotype VIII group B streptococcal infections in Denmark.

28 : Group B streptococcal bacteremia in men.

29 : Balanitis caused by group B streptococcus.

30 : A late sternal wound infection caused by hematogenous spread of bacteria.

31 : Group B streptococcal necrotizing fasciitis and streptococcal toxic shock-like syndrome in adults.

32 : Necrotizing fasciitis and toxic shock-like syndrome caused by group B streptococcus.

33 : Report of 2 fatal cases of adult necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae.

34 : Group B streptococcal disease in nonpregnant adults.

35 : Group B streptococcal sepsis in adults and infants. Contrasts and comparisons.

36 : Group B streptococcal infections in elderly adults.

37 : Clinical and microbiologic features of urethritis in men in Toulouse, France.

38 : Acute prostatitis with prostatic abscess caused by group B Streptococcus.

39 : Streptococcus agalactiae: an emerging cause of septic arthritis.

40 : Streptococcus agalactiae (group B) endocarditis--a description of twelve cases and review of the literature.

41 : Streptococcus agalactiae infective endocarditis: analysis of 30 cases and review of the literature, 1962-1998.

42 : Clinical profile of Streptococcus agalactiae native valve endocarditis.

43 : Tricuspid valve group B streptococcal endocarditis following elective abortion.

44 : Group B streptococcal meningitis complicating elective abortion: report of 2 cases.

45 : Group B streptococcal meningitis in adults: recent increase in Southeast Asia.

46 : Group B streptococcal meningitis in adults: report of twelve cases and review.

47 : Group B Streptococcus endogenous endophthalmitis : case reports and review of the literature.

48 : Serious infections in adults due to group B streptococci. Clinical and serotypic characterization.

49 : Group B streptococcus bacteremia in nonpregnant adults.

50 : Supraglottitis due to group B streptococcus in an adult with IgG4 and C2 deficiency: a case report and review of the literature.

51 : The gut as a source of the haemolytic streptococci causing infection in surgery of the intestinal and biliary tracts.

52 : Mycotic aneurysm caused by group B streptococcus: a cautionary tale of management problems and a rare organism.

53 : Group B streptococcal infection of a pacemaker wire following sigmoidoscopy.

54 : Group B streptococcal toxic shock-like syndrome: report of a case and purification of an associated pyrogenic toxin.

55 : Group B streptococcus toxic shock-like syndrome in a healthy woman: a case report.

56 : Evaluation of streptococcal toxic shock-like syndrome caused by group B streptococcus in adults in Japan between 2009 and 2013.

57 : Antimicrobial susceptibilities of group B streptococci isolated between 1992 and 1996 from patients with bacteremia or meningitis.

58 : Frequent resistance of clinical group B streptococci isolates to clindamycin and erythromycin.

59 : Frequency of antimicrobial resistance among invasive and colonizing Group B streptococcal isolates.

60 : High rates of erythromycin and clindamycin resistance among OBGYN isolates of group B Streptococcus.

61 : High rates of perinatal group B Streptococcus clindamycin and erythromycin resistance in an upstate New York hospital.

62 : Clinical and bacterial features of Group B streptococci with reduced penicillin susceptibility from respiratory specimens: a case-control study.

63 : Molecular epidemiology of macrolide resistance in neonatal bloodstream isolates of group B streptococci.

64 : Fluoroquinolone-resistant Streptococcus agalactiae: epidemiology and mechanism of resistance.

65 : Characterization of fluoroquinolone-resistant beta-hemolytic Streptococcus spp. isolated in North America and Europe including the first report of fluoroquinolone-resistant Streptococcus dysgalactiae subspecies equisimilis: report from the SENTRY Antimicrobial Surveillance Program (1997-2004).

66 : High prevalence of fluoroquinolone-resistant group B streptococci among clinical isolates in China and predominance of sequence type 19 with serotype III.

67 : Multiclonal emergence of levofloxacin-resistant group B Streptococcus, Taiwan.

68 : High isolation rate of MDR group B streptococci with reduced penicillin susceptibility in Japan.

69 : Fluoroquinolone-Resistant Streptococcus agalactiae Invasive Isolates Recovered in Argentina.

70 : Invasive group B Streptococcus isolates showing reduced susceptibility to penicillin in Hong Kong.

71 : Low but Increasing Prevalence of Reduced Beta-lactam Susceptibility Among Invasive Group B Streptococcal Isolates, US Population-Based Surveillance, 1998-2018.

72 : Relatively high rates of cefotaxime- and ceftriaxone-non-susceptible isolates among group B streptococci with reduced penicillin susceptibility (PRGBS) in Japan.

73 : Two cases of invasive vancomycin-resistant group B streptococcus infection.

74 : Relapsing invasive group B streptococcal infection in adults.

75 : Clinical and microbiological characteristics of recurrent group B streptococcal infection among non-pregnant adults.

76 : Incidence of invasive Group B Streptococcus (iGBS) infections and the factors associated with iGBS mortality in adults during 2013-2017: a retrospective study at Thailand's largest national tertiary referral center.

77 : Invasive Group B Streptococcus Infections in Adults, England, 2015-2016.

78 : Group B streptococcal bacteraemia in the elderly.

79 : Group B streptococcal bacteremia in non-pregnant adults: results from two Korean centers.