Infections due to the <i>Streptococcus anginosus </i>(<i>Streptococcus milleri</i>) group

Infections due to the Streptococcus anginosus (Streptococcus milleri) group

Authors:: Jason Stout, MD; Kristen Dicks, MD, MPH
Section Editor:: Daniel J Sexton, MD
Deputy Editor:: Milana Bogorodskaya, MD

Literature review current through: Jan 2024.

This topic last updated: Aug 24, 2022.

INTRODUCTION — The Streptococcus anginosus group (also known as the Streptococcus milleri group) is a subgroup of viridans streptococci that consists of three distinct streptococcal species: S. anginosus, Streptococcus intermedius, and Streptococcus constellatus. These organisms are part of the normal human flora colonizing the oropharynx, gastrointestinal tract, and vagina [1-3].

The microbiology, pathogenesis, sites of clinical infection, diagnostic evaluation, and overview of management of infections caused by members of the S. anginosus group in both adults and children will be reviewed here.

Specifics of diagnosis, antimicrobial regimens, and duration of therapy for a particular infectious syndrome caused by S. anginosus group is discussed elsewhere. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections" and "Complications, diagnosis, and treatment of odontogenic infections" and "Deep neck space infections in adults" and "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Treatment and prognosis of bacterial brain abscess" and "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults" and "Management and prognosis of parapneumonic pleural effusion and empyema in adults" and "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children" and "Management and prognosis of parapneumonic effusion and empyema in children" and "Pyogenic liver abscess" and "Antimicrobial therapy of left-sided native valve endocarditis" and "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis" and "Nonvertebral osteomyelitis in adults: Treatment" and "Vertebral osteomyelitis and discitis in adults" and "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Prosthetic joint infection: Treatment".)

MICROBIOLOGY — S. anginosus was originally differentiated into six groups on the basis of Gram stain morphology, hemolysis on sheep agar plates, and metabolic characteristics [4]. Although the members comprising the S. anginosus group have been called various names (eg, S. MG [5], S. milleri [6], Streptococcus intermedius, and Streptococcus constellatus [7]), modern sequencing-based techniques recognize three distinct species in the S. anginosus (also called S. milleri) group: S. anginosus, S. intermedius, and S. constellatus [8]. S. constellatus has been divided into three subspecies (constellatus, pharynges, and viborgensis) and S. anginosus has been divided into two subspecies (anginosus and whileyi) [8]; the clinical relevance of these divisions remains unknown.

The S. anginosus spp are gram-positive, catalase-negative facultative anaerobic cocci that form small colonies on agar media. They are members of the S. viridans group. The phenotypic characteristics of these organisms vary; most strains demonstrate alpha-hemolysis on blood agar but some may demonstrate beta-hemolysis or no hemolysis at all [9]. The isolates exhibiting beta-hemolysis may carry Lancefield group antigens (eg, group A, C, F, or G); in one study, 18 out of 30 isolates carried Lancefield group antigens [10,11]. These organisms are typically distinguished from other Group C and G streptococci due to their small colony size. (See "Group C and group G streptococcal infection", section on 'Microbiology'.)

Commercially available automated systems that rely on metabolic profiles have historically performed poorly in identifying S. anginosus group organisms and correctly assigning species within this group; more modern systems that employ matrix-assisted laser desorption/ionization-time of flight or multilocus gene sequencing are necessary for accurate assignment to the S. anginosus group and species identification [12,13].

PATHOGENESIS — Although organisms in the S. anginosus group frequently colonize the oropharyngeal and gastrointestinal tracts without harm to the host [14-17], they can also cause invasive disease. A number of putative virulence factors have been identified, including fibronectin-binding protein [18], hyaluronidase, ribonucleases, deoxyribonucleases, and chondroitin sulfatase [19], but their role in human infection is unclear. Over 70 potential virulence genes have been identified in S. intermedius, and one analysis suggested that possession of specific clusters of genes was associated with specific sites of disease [20]. For example, organisms isolated from brain or pulmonary abscesses possessed a different cluster of virulence genes compared with organisms isolated from liver or abdominal abscesses. Whether this clustering represents site-directed virulence or an epiphenomenon remains unknown.

Some of these organisms may also have polysaccharide capsules that inhibit neutrophil phagocytosis [21].

Synergistic interactions with other organisms such as anaerobes and other oral commensals may play an important role in the pathogenesis of the S. anginosus group [22-25]. In one mouse model study, the presence of a capsule or inoculation with a “helper” organism were associated with abscess formation [26], suggesting that there may be multiple pathogenic factors that lead to this common clinical manifestation.

SITES OF CLINICAL INFECTION

Spectrum of disease — Members of the S. anginosus group have been associated with infections at a wide variety of sites including skin/soft tissue, oropharynx, abdomen, brain, and respiratory tract [27-29]. These infections span a wide range of severity from minor tooth abscesses to severe sepsis. Invasive disease often is associated with trauma or comorbidities such as diabetes or malignancy [3]. Polymicrobial infection with anaerobes or other gram-negative gastrointestinal tract commensals is common. Abscess is a prominent manifestation of these infections and should always be considered if not apparent on initial evaluation.

The clinical presentation of specific sites of infection is discussed in the following sections. Management of S. anginosus infections is discussed separately. (See 'Management' below.)

Oral and oropharyngeal infections — S. anginosus group organisms are part of the normal oral flora. They are known to cause dental abscesses and have been associated with pharyngitis and tonsillitis, although distinguishing colonization of the tonsils and pharynx from infection is challenging.

●Dental infections − S. anginosus has been found in dental biofilms and demonstrated in vitro to be capable of dissolving calcium from teeth, a key step in tooth decay [30]. Dental abscesses, often associated with tooth decay, trauma, or dental surgery, are commonly associated with S. anginosus group organisms. For example, one retrospective study of 184 consecutive patients presenting for surgical drainage of dental abscess reported that of 78 patients with positive abscess cultures, 42 (54 percent) grew S. anginosus spp [31]. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections" and "Complications, diagnosis, and treatment of odontogenic infections".)

●Oropharyngeal infections − The role of S. anginosus in pharyngitis and tonsillitis is controversial as the organisms are often part of the normal oropharyngeal flora and determining whether one of these organisms is the true pathogen is difficult. However, there has been at least one study demonstrating that college students with pharyngitis who did not have group A streptococcus isolated from throat cultures were more likely to have S. anginosus isolated from throat cultures than those without pharyngitis [32]. Furthermore, S. anginosus and S. constellatus can be beta-hemolytic and confused with other beta-hemolytic streptococci (eg, Streptococcus pyogenes) in throat cultures [33]. (See "Acute pharyngitis in children and adolescents: Symptomatic treatment" and "Symptomatic treatment of acute pharyngitis in adults" and "Peritonsillar cellulitis and abscess".)

Head and neck infections — S. anginosus group organisms are a common cause of peritonsillar abscess, often accompanied by other oral commensals including anaerobes [3,34,35]. Peritonsillar abscess may lead to local complications such as parapharyngeal abscess, upper airway obstruction, necrotizing fasciitis, mediastinitis, or involvement of other local structures such as the common carotid artery or internal jugular vein (Lemierre syndrome) [36]. Systemic complications, particularly sepsis and brain abscess, have also been well described. (See "Peritonsillar cellulitis and abscess" and "Deep neck space infections in adults" and "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein".)

Cervical necrotizing fasciitis, which often occurs as a complication of dental or pharyngeal infection, is typically polymicrobial and often includes S. anginosus group organisms. One series reported that 39 out of 59 (66 percent) patients with cervical necrotizing fasciitis had S. anginosus group organisms isolated from operative cultures [37]. Ludwig angina, a rapidly progressive cellulitis involving the floor of the mouth, has a similar microbiology to cervical necrotizing fasciitis and may evolve into necrotizing fasciitis or mediastinitis [38]. (See "Ludwig angina".)

S. anginosus group organisms have been increasingly noted in children with severe otitis media and/or sinusitis complicated by epidural abscess, cerebritis, meningitis, and subdural empyema [39,40]. For unclear reasons, the incidence of these infections attributed to S. anginosus group has increased over time at several centers [39,41,42]. (See "Acute otitis media in children: Clinical manifestations and diagnosis" and "Acute bacterial rhinosinusitis in children: Clinical features and diagnosis", section on 'Complications'.)

Central nervous system infections — S. anginosus group organisms are major causes of central nervous system abscesses, including brain abscess, epidural abscess, and subdural empyema, in adults and children [43-46]. They can also cause meningitis or cavernous venous thrombosis [47]. These infections may occur due to direct extension from nearby structures (sinuses, internal ear), postoperatively, or as a complication of hematogenous infection. In cases without direct extension, the primary bacteremia may have resolved by the time of presentation, making the microbiologic diagnosis more challenging. Immunodeficiency and congenital heart disease are commonly cited as underlying risk factors for these infections [45]. Prompt imaging and drainage are cornerstones of both diagnosis and management of these infections [48,49]. (See 'Management' below and "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Treatment and prognosis of bacterial brain abscess" and "Intracranial epidural abscess" and "Bacterial meningitis in children older than one month: Clinical features and diagnosis" and "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Septic dural sinus thrombosis".)

Thoracic infections — Thoracic infections due to S. anginosus group organisms range from aspiration pneumonia to deep tissue infections such as mediastinitis and empyema. Most of the patients have underlying comorbidities [50].

●Pneumonia – S. anginosus group organisms likely play a significant role in aspiration pneumonia [51,52]. Community-acquired pneumonia due to S. anginosus group organisms is relatively uncommon [53-55], although the prevalence may be underestimated by conventional culture methods [56]. Published cases frequently depict the more severe end of the pneumonia spectrum with extensive lung necrosis [57]. (See "Aspiration pneumonia in adults".)

●Lung abscesses and pleural space infections – S. anginosus group organisms play a prominent role in lung abscesses and pleural space infections (eg, empyema). These infections are the most common intrathoracic manifestation of S. anginosus infection. They are often part of a polymicrobial infection and are found in conjunction with anaerobes [22,50,52,58,59]. In one study employing 16S ribosomal ribonucleic acid (rRNA) next-generation sequencing to examine the etiology of pleural fluid samples in 243 patients, S. anginosus group bacteria were detected in 29 percent of samples, often in concert with oral anaerobes [60]. Another large cohort demonstrated a similar prominence of S. anginosus in pleural infections, particularly in community-acquired infections [61]. The presence of S. anginosus was associated with better one-year survival after these infections, particularly compared with Staphylococcus aureus or Enterobacteriaceae [60,61]. (See "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children" and "Management and prognosis of parapneumonic effusion and empyema in children" and "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults" and "Management and prognosis of parapneumonic pleural effusion and empyema in adults" and "Lung abscess in adults".)

●Mediastinitis − A particularly severe thoracic manifestation of S. anginosus group infection is mediastinitis. This may be a descending infection due to a dental or oropharyngeal infection [38,62] or a postoperative complication [63]. Patients with descending infection may present with stridor and neck swelling with progressive development of chest pain, dyspnea, and subcutaneous emphysema. Urgent surgical consultation is crucial for management of these unusual cases. (See "Postoperative mediastinitis after cardiac surgery".)

Abdominal infections — Intra-abdominal infections are a common manifestation of S. anginosus organisms due to their normal colonization of the gastrointestinal tract.

●Liver abscesses − Liver abscesses are common manifestations of S. anginosus group infections; in many series, these organisms are the most common etiology of liver abscess, often in conjunction with Enterobacteriaceae or gut anaerobes [64-66]. Patients typically present with fever and right upper quadrant pain but these symptoms may be frequently absent [66,67]. Biliary tract pathology or instrumentation, gastrointestinal tract pathology (diverticulitis, malignancy), and comorbidities such as diabetes mellitus are risk factors for liver abscess, but there are no risk factors or aspects of the clinical presentation specific for S. anginosus group organisms as opposed to other common causes of liver abscess such as Klebsiella or Escherichia coli [68,69]. Presence of liver abscesses associated with S. anginosus without known abdominal pathology may be indicative of an occult gastrointestinal malignancy [70]. (See "Pyogenic liver abscess".)

●Intra-abdominal abscesses − Intra-abdominal abscesses associated with S. anginosus group organisms may be related to primary abdominal pathology (eg, perforation due to diverticulitis, malignancy, or appendicitis), postoperative, or metastatic complications of bacteremia [71-74]. These infections are almost always polymicrobial and contain other typical enteric flora [75]. Intra-abdominal abscesses associated with S. anginosus without known antecedent abdominal pathology may be a sign of occult gastrointestinal malignancy [70].

●Cholangitis − Cholangitis, particularly in the setting of anatomic abnormalities of the biliary tree or post-transplantation [76], is another setting in which S. anginosus group bacteria may be encountered. S. anginosus group organisms are prominent colonizers of biliary stents and their presence in stent biofilms is positively correlated with the presence of Fusobacterium, a key copathogen [17]. Recurrent cholangitis with these organisms after abdominal organ transplantation has been reported [76].

Bacteremia — Unlike other viridans streptococci, S. anginosus group organisms rarely represent contaminants when isolated from blood cultures [77,78]. Within the S. anginosus group, S. anginosus may be more likely to cause bacteremia than S. constellatus or S. intermedius [28,79]. S. anginosus group bacteremia is often associated with a focal site of infection; isolated bacteremia without another identified site of infection has been reported in only 9 to 16 percent of cases [29,77]. Polymicrobial bacteremia is common and often associated with an underlying abscess [77]. The mortality rate of S. anginosus group bacteremia has ranged between 10 and 16 percent [78,80-83].

Because S. anginosus group organisms are not common causes of endocarditis, we do not routinely perform echocardiograms on all patients with bacteremia due to these organisms. For patients with bacteremia due to members of the S. anginosus group, we generally obtain echocardiography in patients with a prosthetic valve, those with persistent (>48 hours) bacteremia despite appropriate antibiotic therapy, and those who meet Duke criteria for possible endocarditis. If transthoracic echocardiography does not demonstrate findings consistent with endocarditis, then a transesophageal echocardiogram should be performed.

Endocarditis — Endocarditis due to the S. anginosus group is uncommon [84-87], typically representing <10 percent of endocarditis due to viridans streptococci [88], and bacteremia with these organisms is far less likely to be associated with endocarditis than bacteremia with S. mitis [85,89]. The presentation of endocarditis due to S. anginosus group is similar to that of other viridans streptococci [86,87,89]. S. anginosus seems more likely to cause endocarditis as compared with S. intermedius and S. constellatus [84,85].

Soft tissue/osteoarticular infections — Skin and soft tissue infections (SSTIs) are a common presentation of S. anginosus group infections [90,91]. SSTIs can present as cellulitis, infected sacral decubitus ulcers, surgical site infections, focal abscesses, and necrotizing fasciitis [3,91]. Bacteremia is often present [29] and these infections are frequently polymicrobial [91].

Bone and joint infections due to the S. anginosus group are relatively uncommon. Direct extension of infection to the bones of the skull as a result of odontogenic or sinus infection may be the most frequently reported cause of osteomyelitis due to these organisms [42,92]. Patients may present with mastoiditis, Pott puffy tumor, or extension to the cervical vertebrae [93]. Chronic osteomyelitis of the mandible due to members of the S. anginosus group has been reported in several patients after dental implants [94]. Local extension of soft tissue infection to underlying bone, particularly in patients with diabetic foot ulcers, is another common mechanism for osteomyelitis [92]. Hematogenous seeding of bone is probably the least common cause of osteomyelitis due to S. anginosus group organisms but has been reported [95,96]. Infections due to direct extension, either from a head/neck source or a wound, are frequently polymicrobial [92,93,97]. As with other focal S. anginosus group infections, concomitant bacteremia is frequently encountered [92].

DIAGNOSTIC EVALUATION

When to suspect S. anginosus — Clinically, infection with S. anginosus group organisms cannot be distinguished from other bacterial pathogens that cause similar infectious syndromes. However, due to the characteristic pyogenic nature of this group of bacteria, the presence of an abscess (especially within the head/neck or abdomen) should increase suspicion for S. anginosus infection.

Establishing the diagnosis — Unlike less virulent members of the viridans streptococci, members of the S. anginosus group should generally be considered true pathogens when isolated from blood, percutaneous aspirates from abscesses, or other sterile sites [98-100]. Isolation of these organisms from wounds may indicate true infection or colonization and should be interpreted in the clinical context of the patient. Isolation from urine, indwelling abdominal/biliary drains, or decubitus ulcers without clinical evidence of acute infection likely represents colonization rather than infection [101].

S. anginosus group organisms can often be identified using routine, phenotype-based culture systems, although misidentification is not rare. Definitive identification, including species designation, typically requires techniques such as matrix-assisted laser desorption/ionization-time of flight or gene sequencing [12,13,102]. When cultures are negative but S. anginosus infection is suspected (particularly in the setting of prior antibiotic therapy), 16S rRNA gene sequencing may be useful in identification of S. anginosus from culture-negative abscesses [103].

Given the high prevalence of concurrent infection with anaerobic organisms, we make sure to collect appropriate specimens for anaerobic culture as well [104,105]. Polymicrobial infection, particularly with other oral anaerobes (eg, Fusobacterium spp), is common and probably underestimated using standard culture techniques; molecular techniques may be more sensitive in detecting copathogens [22,52,60,77,106].

Evaluation for abscesses — Identification of S. anginosus group organisms on culture should prompt further evaluation for abscesses, both distal and near the source of infection. Detection of abscesses is critical in the management of this infection, as all abscesses should be drained, if possible. (See 'Management of abscesses' below.)

Positive blood cultures should prompt evaluation for focal suppurative infection, which should include a careful history and physical exam that guide the choice of appropriate imaging studies to evaluate for intraabdominal abscess, deep-seated head and neck infection, brain abscess, and/or endocarditis [14,46,77,78,80,107-109] (see 'Bacteremia' above). However, occasionally, brain abscesses, intraabdominal and liver abscesses, and empyema can be occult [49,74,91,110-112]. Given the high prevalence of abdominal pathology in patients with S. anginosus bacteremia [101,107], we obtain abdominal imaging (computed tomography or magnetic resonance imaging) in patients who have bacteremia without a clear clinical focus of infection.

Conversely, deep-seated infections due to S. anginosus group (eg, head and neck infections) should prompt collection of blood cultures. If no abscess is clinically apparent at the site of infection, careful monitoring is warranted to detect early development of abscess [80,113,114].

MANAGEMENT — In general, treatment of infections caused by members of the S. anginosus group consists of abscess drainage/debridement (if feasible) and antimicrobial therapy [115].

Antimicrobial therapy

Antimicrobial resistance — Susceptibility testing practices vary widely among clinical laboratories; some laboratories do not routinely perform susceptibility testing since the majority of isolates are susceptible to penicillin G (minimum inhibitory concentrations [MICs] ≤0.125 mcg/mL) [116,117]. Less than two percent of S. anginosus group strains are penicillin intermediate (MICs between 0.25 and 2 mcg/mL) and penicillin-resistant (MIC ≥4 mcg/mL) [3]. Such penicillin-intermediate or -resistant strains have altered penicillin-binding proteins and are more likely to be S. anginosus or S. intermedius than S. constellatus. Penicillin-intermediate or resistant strains rarely cause treatment failure [3].

Penicillin susceptibility typically connotes susceptibility to third-generation cephalosporins, but rare isolates that are susceptible to penicillin but resistant to ceftriaxone have been reported [118]. Since these cases are rare, we do not routinely test for ceftriaxone resistance.

S. anginosus group organisms are typically susceptible in vitro to vancomycin, linezolid, tedizolid, and daptomycin [119-122]. However, resistance to daptomycin develops easily so we do not use daptomycin for treatment of these organisms [119].

Fluoroquinolone MICs among S. anginosus group members are often in the susceptible range. However, as resistance tends to develop easily, fluoroquinolones are not appropriate for treatment of patients with infections due to these organisms [123,124].

Macrolide resistance has also emerged in members of the S. anginosus group; thus macrolide therapy is not recommended [116,122,125,126].

Most strains of the S. anginosus group are resistant to aminoglycosides [87,127]; sulfonamides and tetracyclines have no activity against S. anginosus group isolates.

Antibiotic selection — Most patients with S. anginosus infection warrant initial treatment with intravenous antibiotics. The exception is minor oral and endodontic infections that may respond to extraction of an infected tooth and/or abscess drainage together with oral antimicrobial therapy.

The S. anginosus group is susceptible to all beta-lactams. Ceftriaxone (2 g intravenously every 24 hours) is our preferred antimicrobial agent due to excellent tissue penetration and ease of dosing, although penicillin G or ampicillin-sulbactam are reasonable alternatives. If allergy or resistance precludes use of beta-lactam agents, vancomycin or linezolid are appropriate alternative agents. Since S. anginosus group infections are often polymicrobial, we favor adding empiric treatment against anaerobes when treating most S. anginosus group infections; exceptions include isolated endovascular infections with no identified abscess after thorough evaluation.

Clinical data comparing the various antibiotic regimens is scarce. However, ceftriaxone appears to be as effective as penicillin G in the treatment of serious S. anginosus infections. In one study of 94 patients with viridans streptococci bacteremia (16 with S. anginosus group organisms), there was no difference in mortality or adverse effects in patients treated with ceftriaxone compared with penicillin G [128].

Anaerobes are known to be copathogens in S. anginosus group infections, especially when abscesses are present [22,80,106]. However, anaerobes are difficult to detect by routine culture methods. As an example, in a retrospective study of 12 patients with empyema due to S. anginosus group organisms, obligate anaerobes were detected in 67 percent of cases by clone gene sequencing compared with 16 percent by standard culture [106].

Daptomycin, fluoroquinolones, macrolides, sulfonamides, and tetracyclines should not be used for the treatment of S. anginosus group organisms. (See 'Antimicrobial resistance' above.)

Initial intravenous regimen — Most patients with S. anginosus infection warrant initial treatment with intravenous antibiotics. Treatment against anaerobes (even if not isolated) should be administered for most patients presenting with S. anginosus group infections [40,115,129]. An exception is isolated S. anginosus group bacteremia or endocarditis with no identified abscess after thorough evaluation that includes cross-sectional imaging (eg, computed tomography, magnetic resonance). Antianaerobic treatment is usually achieved by adding metronidazole to ceftriaxone or treating with either a beta-lactam-beta-lactamase inhibitor combination or a carbapenem (table 1).

Preferred options for antimicrobial regimens include (refer to table for dosing in children) (table 2):

●Ceftriaxone 2 g intravenously every 24 hours PLUS metronidazole 500 mg orally or intravenously every 8 hours.

●Ampicillin-sulbactam 3 g intravenously every six hours.

●Penicillin G (2 to 4 million units intravenously every four to six hours) PLUS metronidazole 500 mg orally three times daily. Penicillin G is an alternative to ceftriaxone but is not more effective that ceftriaxone and is more challenging to dose.

Alternative options for patients who cannot tolerate penicillins or cephalosporins include:

●For patients who require antianaerobic therapy: Ertapenem 1 g intravenously every 24 hours

●For patients with endovascular infections without associated abscess: Vancomycin intravenously (refer to tables for dosing in adults (table 3) and children (table 4)) or linezolid 600 mg intravenously or orally twice a day

For patients with a beta-lactam allergy, the severity and characteristics of the allergy should be assessed to determine whether the patient can receive penicillins, cephalosporins, or carbapenems. (See "Choice of antibiotics in penicillin-allergic hospitalized patients".)

Infections in the central nervous system (CNS) warrant higher doses of ceftriaxone (2 g IV every 12 hours) or penicillin G (4 million units every 4 hours) to ensure adequate penetration through the blood brain barrier.

Oral step-down regimens for select cases — For patients who were initiated on an intravenous regimen, oral step-down therapy following initial clinical improvement and source control may be appropriate for certain clinical syndromes (eg, abscess in the absence of bacteremia). Oral step-down therapy regimens include (refer to table for dosing in children) (table 2):

●Amoxicillin-clavulanate 875/125 mg orally twice a day.

●Cefuroxime 500 mg orally twice a day or linezolid 600 mg orally twice a day (linezolid should be reserved for patients with severe beta-lactam allergies and should be administered with another antimicrobial agent with activity against aerobic gram-negative gut flora) (table 2).

PLUS

Metronidazole 500 mg orally three times daily or clindamycin 150 to 450 mg orally three or four times daily.

Because of less favorable pharmacodynamics of typically used oral beta-lactam step-down regimens, we favor continuing the initial intravenous therapy for the entire course in CNS and endovascular infections (eg, CNS abscess, bacteremia, endocarditis).

Duration of therapy — The duration of therapy depends on the underlying site of infection and the ability to obtain source control of concurrent abscesses. In general, antimicrobial therapy should be administered until clinical signs and/or radiologic features of infection have resolved and as recommended for the site of infection.

In the absence of endocarditis, S. anginosus infections have a reasonably good prognosis [77,78,80,81]. Intravenous antimicrobial therapy for an uncomplicated bacteremia should continue for two weeks. Presence of an inadequately drained abscess or other difficult to treat syndromes (eg, endocarditis, osteomyelitis) typically warrant longer courses and re-evaluation of source control.

In the setting of multiple small abscesses not amenable to percutaneous drainage, prolonged antimicrobial therapy (up to six to eight weeks) with close monitoring may be required for cure.

Management of abscesses — In general, treatment of abscesses caused by members of the S. anginosus group requires abscess drainage (if feasible) and antimicrobial therapy for cure [77,80,81,115,130,131]. These infections can be difficult to treat and may require surgical debridement if abscesses cannot be completely drained percutaneously and/or do not resolve with appropriate antimicrobial therapy [131]. For example, in a single-center observational study of 39 patients presenting with S. anginosus empyema, surgical intervention was associated with decreased mortality (0 versus 23 percent), greater discharge to home (77 versus 16 percent), and shorter hospital length of stay (24 versus 34 days) compared with patients who did not undergo surgical intervention [131].

SUMMARY AND RECOMMENDATIONS

●Microbiology − The Streptococcus anginosus group (also known as the Streptococcus milleri group) is a subgroup of viridans streptococci that consists of three distinct streptococcal species: Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus. (See 'Microbiology' above.)

●Sites and severity of clinical infection − The S. anginosus group are part of the normal human flora colonizing the oropharynx, gastrointestinal tract, and vagina. Infection spans a wide range of severity and occurs at a wide variety of sites, including skin/soft tissue, oropharynx, abdomen, brain, and respiratory tract. The S. anginosus group also frequently causes focal polymicrobial abscesses, which can be subtle in presentation. (See 'Sites of clinical infection' above.)

●Diagnostic evaluation

•When to suspect S. anginosus group organisms − Although S. anginosus group organisms cannot be distinguished clinically from other bacterial pathogens that cause similar infectious syndromes, the presence of an abscess (especially within the head/neck or abdomen) should increase suspicion for S. anginosus infection. (See 'When to suspect S. anginosus' above.)

•Microbiologic diagnosis – When members of the S. anginosus group are isolated from blood, percutaneous aspirates from abscesses, or other sterile sites, they should generally be considered true pathogens. Isolation of these organisms from wounds or urine may indicate infection or colonization and should be interpreted in the clinical context of the patient. Anaerobic cultures should be collected given the high prevalence of concurrent infection with anaerobic organisms. (See 'Establishing the diagnosis' above.)

•Evaluation for abscesses − Identification of S. anginosus group organisms on microbiologic testing should prompt further evaluation for abscesses, both distal and near the source of infection. (See 'Evaluation for abscesses' above.)

●Management − Treatment of infections caused by members of the S. anginosus group consists of abscess drainage/debridement (if feasible) and antimicrobial therapy. (See 'Management' above.)

•Antimicrobial therapy

-The S. anginosus group is susceptible to all beta-lactams; we suggest including antianaerobic therapy as part of the antimicrobial regimen for S. anginosus group infections because coinfection with anaerobes is common (Grade 2C) (table 1). An exception is isolated bacteremia and endocarditis with no identified abscess after thorough evaluation that includes cross-sectional imaging (eg, computed tomography, magnetic resonance); these infections are typically monomicrobial and do not necessitate anti-anaerobic therapy. (See 'Antibiotic selection' above.)

-Preferred initial intravenous regimens include ceftriaxone, penicillin G, or ampicillin-sulbactam. Oral step-down regimens include amoxicillin-clavulanate alone or a second- or third-generation cephalosporin plus metronidazole (table 2). (See 'Initial intravenous regimen' above and 'Oral step-down regimens for select cases' above.)

•Duration of antimicrobial therapy − The duration of treatment is guided by the site of infection and the ability to obtain source control. (See 'Duration of therapy' above.)

•Management of abscesses – All abscesses amenable to drainage should be percutaneously drained. If abscesses cannot be completely drained percutaneously and do not improve with appropriate antimicrobial therapy, prompt surgical debridement may be needed to minimize morbidity and mortality. (See 'Management of abscesses' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Charles W Stratton, MD, who contributed to earlier versions of this topic review.

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Topic 3178 Version 34.0

خرید پکیج

Infections due to the Streptococcus anginosus (Streptococcus milleri) group

References