Streptococcus species

Michael Melia, M.D.

MICROBIOLOGY

  • Nomenclature and taxonomy of streptococci are confusing because of many historical efforts at describing the class.
  • Often described by 5% sheep blood agar hemolysis (1902) or Lancefield carbohydrate group antigens (1933).
  • Broadly organized into two groups by hemolysis [Fig. 1], Lancefield and phenotype testing (1937):
    1. Pyogenic (beta-hemolytic), including Groups A, B, C, E, F & G.
      • Group A streptococci: cause complete hemolysis/lysis of red cells in blood agar media around/under colonies caused by streptolysin (exotoxin), so-called β-hemolysis.
        • See the separate module for details on this organism.
    2. Viridans group
      • Usually yield α-hemolysis on blood agar (green surrounding colony - hence name, viridans); may be β-hemolytic or non-hemolytic (latter sometimes termed γ-hemolysis).
  • Other organisms previously classified as Streptococci are now separate genera:
    • Lactococci: generally not human pathogens.
    • Enterococci: see separate module
    • Streptococcal-like, catalase-negative, Gram-positive cocci.
      • e.g., Leuconostoc, Pediococcus
    • Formerly called nutritionally-variant Streptococci
      • Abiotrophia, Granulicatella
  • 16S rRNA gene sequencing (1990s) yields true phylogenetic relationships. Facklam classification presented here[22]

Frequently used designations:

  • Group A streptococci: S. pyogenes (see separate pathogen module)
  • Group B streptococci (S. agalactiae):
    • Found in GI/GU tracts in 10-30% of women. Common in adults >65 and those with comorbidities.
    • Causes one-third of neonatal sepsis/pneumonia/meningitis; also puerperal sepsis, chorioamnionitis, peripartum endometritis, bacteremia (often without clear source), skin and soft-tissue infections, septic arthritis, pneumonia, endocarditis, osteomyelitis.
  • Groups C, F, G streptococci: bacteremia, endocarditis, septic arthritis, osteomyelitis, pharyngitis, skin and soft tissue infections, meningitis, puerperal infection, neonatal sepsis.
    • Nearly all group C/G infections are caused by S. dysgalactiae subsp. equisimilis; manifestations are largely similar to those of S. pyogenes
    • The incidence of such infections is increasing, particularly among elderly persons
  • Group D streptococci (non-enterococcal, e.g., S. gallolyticus subsp. gallolyticus (formerly S. bovis biotype I): associated with colonic malignancy and hepatobiliary disease. Cause of endocarditis.
  • S. intermedius/S. anginosus/S. constellatus group (microaerophilic strep; "S. milleri" no longer appropriate): propensity for invasion, meningitis, abscess production (e.g., head and neck infections), bacteremia, osteomyelitis.
    • Rarely "contaminants" when present in blood cultures.
  • S. suis: zoonotic pathogen associated with pig farming or exposure to contaminated pork products.
    • Most prevalent in Southeast Asia, where it is a common cause of meningitis, hearing loss, cutaneous lesions, and bacteremia/TSS.
    • In the U.S., it may be acquired from feral boars.
  • S. halichoeri: rare pathogen that can be acquired from marine life (initially isolated from gray seals), mammals, and without known animal contacts
    • Can cause bacteremia, empyema, bone & joint infections
  • Viridans Streptococci: oropharynx/GI tracts are the typical niche. Usually α-hemolytic or non-(γ)-hemolytic.
    • Common causes of dental infections, subacute bacterial endocarditis, and bacteremia.
    • If isolated from CSF or respiratory sections, usually contaminants, but occasionally responsible for disease.
    • May also be a common bloodstream contaminant, but needs to be clinically correlated and ruled out as a systemic process, such as endocarditis.
    • Heterogeneous group: may be commensals or pathogens. Little consistency in describing, usually six major groups in the modern era.
      • S. mutans
      • S. salivarius
      • S. anginosus
      • S. mitis
      • S. sanguinis
      • S. bovis
  • Abiotrophia and Granulicatella spp (formerly known as nutritionally-variant streptococci): endocarditis
  • Streptococcus pneumoniae (see separate pathogen module).

CLINICAL

  • Group A streptococci: S. pyogenes (see separate pathogen module)
  • Group B streptococci (S. agalactiae):
    • Found in GI/GU tracts in 10-30% of women. Common in adults >65 and those w/ co-morbidities.
    • Causes one-third of neonatal sepsis/pneumonia/meningitis; also puerperal sepsis, chorioamnionitis, peripartum endometritis, bacteremia (often without clear source), skin and soft-tissue infections, septic arthritis, pneumonia, endocarditis, osteomyelitis.
  • Groups C, F, G streptococci: bacteremia, endocarditis, septic arthritis, osteomyelitis, pharyngitis, skin and soft tissue infections, meningitis, puerperal infection, neonatal sepsis.
    • Nearly all group C/G infections are caused by S. dysgalactiae subsp. equisimilis; manifestations are largely similar to those of S. pyogenes
    • The incidence of such infections is increasing, particularly among elderly persons
  • Group D streptococci (non-enterococcal, e.g., S. gallolyticus subsp. gallolyticus (formerly S. bovis biotype I): associated with colonic malignancy and hepatobiliary disease. Cause of endocarditis.
  • S. intermedius/S. anginosus/S. constellatus group (microaerophilic strep; "S. milleri" no longer appropriate): propensity for invasion, meningitis, abscess production (e.g., head & neck infections), bacteremia, osteomyelitis.
    • Rarely "contaminants" when present in blood cultures.
  • S. suis: zoonotic pathogen associated with pig farming or exposure to contaminated pork products.
    • Most prevalent in southeast Asia, where it is a common cause of meningitis, hearing loss, cutaneous lesions, and bacteremia.
  • S. halichoeri: rare pathogen that can be acquired from marine life (initially isolated from gray seals), mammals, and without known animal contacts
    • Can cause bacteremia, empyema, bone & joint infections
  • Viridans Streptococci: oropharynx/GI tract usual niche. Usually α-hemolytic or non-(γ)-hemolytic.
    • Common cause of dental infections, subacute bacterial endocarditis, bacteremia.
    • If isolated from CSF or respiratory sections, usually contaminants, but occasionally responsible for disease.
    • May also be common bloodstream contaminant, but need to clinically correlate and rule out systemic process such as endocarditis.
    • Heterogeneous group: may be commensals or pathogens. Little consistency in describing, usually six major groups in modern era.
      • S. mutans
      • S. salivarius
      • S. anginosus
      • S. mitis
      • S. sanguinis
      • S. bovis
  • Abiotrophia and Granulicatella spp (formerly known as nutritionally-variant streptococci): endocarditis
  • Streptococcus pneumoniae (see separate pathogen module).

SITES OF INFECTION

  • Blood: primary bacteremia, especially with neutropenia or malignancy
    • Species other than GAS may occasionally cause a toxic shock-like syndrome.
  • Cardiovascular: endocarditis
  • Head and neck: dental infections, deep neck space infections (including submandibular, retropharyngeal and lateral neck)
  • Lung: pneumonia (rare) associated with oropharyngeal aspiration, abscess and empyema
  • Abdomen: abscesses including liver, cholangitis, visceral infections, GU tract
  • Shock syndrome (low BP, rash, ARDS) due to viridans strep (e.g., S. mitis), most frequently described in cancer patients
  • CNS: brain abscess, meningitis
  • Musculoskeletal: septic arthritis, cellulitis, osteomyelitis
  • GI tract: S. gallolyticus subsp. gallolyticus colonizes >55% of patients with colorectal cancer (10% of the normal population)

TREATMENT

General Considerations Regarding Streptococcal Endocarditis

  • See endocarditis module for additional details.
  • Four-week duration of therapy is considered standard. Short course (2 wk) possible if certain criteria are met.
  • Criteria favoring 2-wk short course beta-lactam + aminoglycoside combination for endocarditis:
    1. PCN-sensitive oral viridans Streptococci or S. bovis (PCN MIC < 0.125mg/L).
    2. Native valve endocarditis.
    3. No heart failure, aortic insufficiency or conduction abnormality.
    4. No metastatic infectious foci.
    5. Quick clinical response and afebrile within 7 days.

Viridans Streptococci

  • Cause of primary bacteremia, but up to 80% of cultures may represent contaminants or transient bacteremia.
    • Don’t dismiss in cancer patients on chemotherapy or if neutropenic.
    • Continuous bacteremia → suspect endocarditis.
  • The viridans group is responsible for the declining percentage of endocarditis compared to "enteric" streptococci such as S. gallolyticus subsp. gallolyticus and Enterococci, likely due to an aging population and a decrease in rates of rheumatic heart disease.
    • For endocarditis, use the module of bloodstream isolate for additional therapy specifics.
  • Therapy (AHA 2015 Guideline): β-lactams are preferred therapy.
    • Penicillin G 2-3 million U IV q4h +/- gentamicin for synergy 1.0 mg/kg/q8h IV
    • Ceftriaxone 2 g IV once daily
    • Vancomycin 15 mg/kg IV q12h (if PCN allergic)
    • Others:
      • Tetracyclines, macrolides, clindamycin: avoid for empiric therapy as up to 25-50% isolates are resistant.
      • Note: TMP/SMX >75% resistance rates.
      • Do not be reassured by reported daptomycin susceptibility: Rapid development of high-level daptomycin resistance with daptomycin exposure has been described.
    • There is increasing resistance to beta-lactams with some species, esp. S. mitis (>40%).
  • Duration 10-14 days (not endocarditis).

Streptococcus anginosus group

  • Group comprises 3-15% of streptococcal isolates of endocarditis.
    • See the Endocarditis module for management of this infection, follow the viridans Streptococci recommendations.
  • Non-endocarditis infections: more frequently seen than endocarditis

Group B Streptococcus (S. agalactiae)

  • Treatment:
    • Bacteremia, soft tissue infections: PCN G 10-12 million units/d x 10d (e.g., 2MU q4h or six divided doses/d).
    • Meningitis (adult): PCN G 20-24 million units/d x 14-21d.
    • Osteomyelitis: PCN G 20-24 million units/d x 4-6w.
    • Endocarditis: PCN G 20-24 million units/d x 4-6w AND gentamicin 1mg/kg q8h for first 2 wks.
    • PCN allergic: may substitute vancomycin 15 mg/kg IV q 12h for PCN, although vancomycin resistance has been reported (rare).
      • Avoid clindamycin, given 29% of isolates are resistant in a global meta-analysis.
        • Confirm absence of inducible clindamycin resistance (typically associated with macrolide resistance) before using as monotherapy.
      • Cefazolin is a good alternative in someone with a penicillin allergy, given its unique side chain and very low rates of resistance.
    • Because GBS is slightly more resistant than GAS to penicillin, some add gentamicin (1 mg/kg q8h IV) for any serious GBS infection.
    • Skin and soft tissue infections:
      • Cellulitis (mild): penicillin VK 250-500 mg PO q6h or, if concurrent MSSA infection not excluded, cephalexin 500 mg PO q6h or cefadroxil 500 mg q12h x5d
      • Cellulitis (moderate or severe): PCN 2-4 million units IV q4-6h or (if PCN allergic) cefazolin 1 g IV q8h; alternatives include clindamycin 600-900 mg IV q8h
        • Cellulitis can typically be treated with 5-day antibiotic therapy, provided clinical improvement has occurred
        • Concurrent supportive care measures and treatment of toe web abnormalities (for lower extremity cellulitis) are important.
      • Impetigo (non-bullous, mild): Topical mupirocin BID x 5d
      • Impetigo (non-bullous; many lesions or many persons affected): cefadroxil 500 mg PO q12h x7d or cephalexin 250 mg PO q6h x7d or (if PCN allergic) clindamycin 300-450 mg PO q6h x7d
  • Prevention of perinatal infection:
    • Without intervention, the risk of vertical transmission from a mother colonized with GBS is approximately 50%.
      • 1-2% of these infants will manifest a clinical infection
    • Indications for peripartum antibiotic prophylaxis to prevent early-onset (within seven days of birth) disease:
      • Recovery of GBS from the urine during pregnancy
      • Prior delivery of an infant who sustained invasive GBS disease
      • Positive lower vaginal/rectal swab at 36-37 weeks of gestation (universal screening recommended in many countries, including the U.S., if above criteria not met)
        • No RCT evidence to support this approach, but screening and intervention was associated with a 65% reduction in early-onset GBS disease in the U.S. from 1993-1998
      • If no screen result available, prophylaxis if:
        • < 37 weeks of gestation
          • Compared with infants born at term, pre-term infants have a three-fold increased risk of neonatal sepsis/pneumonia/meningits
        • Fetal membrane rupture ≥18h
        • Intrapartum temperature >38C°
        • Intrapartum NAAT positive for GBS
      • No need for prophylaxis if cesarean delivery prior to rupture of amniotic membranes (as risk of neonatal sepsis is extremely low with cesarean section)
    • Recommended prophylactic regimens:
      • Preferred:
        • Penicillin 5 million units IV x1, then 2.5-3.0 million units IV q4h until delivery
        • Ampicillin 2 grams IV x1, then 1 gram IV q4h
      • PCN allergic (non-anaphylactic, non-urticarial):
      • PCN allergic (anaphylactic or urticarial):
        • Clindamycin 900 mg IV q8h (if isolate confirmed as susceptible) or vancomycin 1 g IV q12h (for clindamycin-resistant strains).
        • D-test should be performed to confirm the absence of inducible clindamycin resistance.
      • Erythromycin is not recommended.
      • Administer at least 2h, and ideally at least 4h, before delivery.

Group D Streptococci

  • Penicillin high-level resistance not described; some strains are resistant to clindamycin.
  • Bacteremia: PCN 12-18 million units IV daily in divided doses x 10-14d.
  • Endocarditis:
    • If highly susceptible to PCN: PCN 12-18 million units/d IV x 4 weeks
      • Consider adding gentamicin 1mg/kg q8h to shorten duration to 2 weeks
    • If PCN MIC >0.12 to < 0.5: PCN 24 MU/d x4w + gentamicin 1 mg/kg q8h x2w
    • If PCN MIC >0.5 (rare): PCN 24 MU/d + gentamicin 1 mg/kg q8h x4-6w
  • For bacteremia or endocarditis: Evaluate the GI tract to exclude malignancy.

Group C, E, F Streptococci:

  • Bacteremia, septic arthritis or other serious infection: PCN 12-18 million units/d IV ± synergistic gentamicin (1 mg/kg IV q8h) x 10-14d.
    • Emergence of high-level aminoglycoside resistance has been described among GGS.
  • Cellulitis (mild): penicillin VK 250-500 mg PO q6h or, if concurrent MSSA infection not excluded, cefadroxil 500 mg PO q12h x5d or cephalexin 500 mg PO q6h x5d
  • Cellulitis (moderate or severe): PCN 2-4 million units IV q4-6h or (if PCN allergic or concurrent MSSA infection not excluded) cefazolin 1 g IV q8h; alternatives include clindamycin 600-900 mg IV q8h
    • Cellulitis can typically be treated with 5 days of antibiotic therapy, provided clinical improvement has occurred.
    • Concurrent supportive care measures and treatment of toe web abnormalities (for lower extremity cellulitis) are important.
  • Endocarditis: see Endocarditis module using viridans streptococci recommendations for specifics.
  • Impetigo (non-bullous, mild): Topical mupirocin or retapamulin twice daily x5d
  • Impetigo (non-bullous; many lesions or many persons affected): cefadroxil 500 mg PO q12h x7d or Cephalexin 250 mg PO q6h x7d or (if PCN allergic) clindamycin 300-450 mg PO q6h x7d.
  • Group C and G Streptococci:
    • Oxacillin and nafcillin are ineffective.
    • Resistance to tetracycline, erythromycin, and fluoroquinolones is described.

Abiotrophia and Granulicatella spp:

  • Mainly a cause of endocarditis.
  • Less susceptible in vitro to PCN than other streptococci.
    • 33-67% of strains are relatively PCN-resistant (MIC 0.25-2.0 µg/mL).
    • Some isolates are highly resistant (MIC ≥4 µg/mL).
  • High-level aminoglycoside resistance has not been reported.
  • See the Endocarditis module using the viridans Streptococci recommendations
    • Would not use 2-week "short-course" therapy for these organisms.

Streptococcus suis

  • Meningitis: Ceftriaxone 2 grams IV q12h x14 days; also consider penicillin G 24 million units/d x10-14 days.
    • Dexamethasone 0.4mg/kg q12h x 4d is the standard recommendation for confirmed bacterial meningitis among adults in Southern Vietnam, as morbidity and mortality have been shown to be reduced with administration.
  • Patients who relapse after two weeks of therapy should receive prolonged treatment (4-6 weeks).

Streptococcus pyogenes (Group A Strep)

Streptococcus pneumoniae (Pneumococcus)

Selected Drug Comments

Drug

Recommendation

Ceftriaxone

Once a day IV/IM cephalosporin with activity against almost all strains of streptococci.

Cephalexin

Active against most streptococci, though lower bioavailability and frequent dosing make it a choice for less serious infections.

Cefadroxil

A good alternative to cephalexin given twice-daily, rather than four-times daily, dosing (with normal renal function)

Clarithromycin

Resistance is not uncommon among many strep species.

Clindamycin

Available in both PO and IV forms. Well tolerated, but high incidence of C. difficile-associated colitis. Not reliably active against viridans Streptococci and GBS.

Erythromycin

Resistance is not uncommon for many species.

Gentamicin

May add for synergy in the setting of endocarditis, serious bacteremia or if PCN MIC > 0.1.

Penicillin

Preferred therapy for susceptible strains of streptococci.

Cefazolin

Given a unique side chain, a good alternative to penicillin in PCN-allergic patients with little risk of anaphylaxis or serious drug reactions.

Vancomycin

Active against nearly all strains of streptococci. Must be given IV. Usually, it is only used in settings of PCN allergy.

Daptomycin

Emergence of resistance to therapy has been described for viridans streptococci.

OTHER INFORMATION

  • Viridans streptococci:
    • A high proportion of blood cultures growing viridans streptococci may be due to cutaneous contamination or transient oral bacteremia.
    • Penicillin-resistance with viridans streptococci is not due to beta-lactamase production (hence no benefit from using agents such as ampicillin/sulbactam).
  • S. anginosus group is especially confusing as it can be either beta-hemolytic or non-hemolytic.
  • Recurrent invasive Group B Streptococcal infection is described in 4% of nonpregnant adults within one year of the first episode.
  • Consider Abiotrophia or Granulicatella (formerly nutritionally-variant strains) in "culture-negative" endocarditis.
    • Special media historically required, though many modern broth micro systems should recover these organisms.
  • While U.S. incidence rates of meningitis caused by pneumococcus, meningococcus, L. monocytogenes, and H. influenzae decreased significantly from 1998-2007, incidence rates for S. agalactiae meningitis (as well as bacterial meningitis incidence rates among infants < 2 months) did not decrease.
  • Collecting vaginal swabs for real-time GBS PCR and culture at the beginning of labor has been studied and may reduce unnecessary antibiotic therapy among previously culture-positive pregnant women; additional studies are needed.

Basis for recommendation

  1. Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of America (IDSA) Clinical Practice Guidelines for the Diagnosis and Treatment of Native Vertebral Osteomyelitis in Adults. Clin Infect Dis. 2015;61(6):e26-46.  [PMID:26229122]

    Comment: Osteomyelitis treatment recommendations are based upon this document.

  2. Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. 2015;132(15):1435-86.  [PMID:26373316]

    Comment: Endocarditis treatment recommendations are based upon this document.

  3. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-52.  [PMID:24973422]

    Comment: Far-reaching, comprenhensive review of skin and soft tissue infections, including those caused by beta-hemolytic Streptococci (with treatment recommendations as noted herein) as well as more common pathogens such as S. pyogenes and S. aureus. Update in progress

References

  1. Hsu CY, Moradkasani S, Suliman M, et al. Global patterns of antibiotic resistance in group B Streptococcus: a systematic review and meta-analysis. Front Microbiol. 2025;16:1541524.  [PMID:40342597]

    Comment: In this meta-analysis including 266 studies from 57 countries, rates of Streptococcus agalactiae resistance to penicillin, ampicillin, and vancomycin resistance remain extremely low. Tetracyclines, macrolides, and clindamycin cannot confidently be used empirically.

  2. Xie O, Davies MR, Tong SYC. Streptococcus dysgalactiae subsp. equisimilis infection and its intersection with Streptococcus pyogenes. Clin Microbiol Rev. 2024;37(3):e0017523.  [PMID:38856686]

    Comment: Review of S. dysgalactiae subsp. equisimilis, which is causing an increasing incidence of infections, particularly among elderly persons, with manifestations similar to those of S. pyogenes. It may more commonly cause endocarditis. Like S. pyogenes, resistance to penicillin remains extremely rare.

  3. Stephens K, Charnock-Jones DS, Smith GCS. Group B Streptococcus and the risk of perinatal morbidity and mortality following term labor. Am J Obstet Gynecol. 2023;228(5S):S1305-S1312.  [PMID:37164497]

    Comment: This review highlights the potential consequences of GBS neonatal sepsis as well as its relative rarity. If 20% of women are colonized, and the risk of vertical transmission in the setting of colonization is 50%, and 1-2% infants manifest clinical infection, 1 in 1000 infants will manifest clinical infection.

  4. Shakir SM, Gill R, Salberg J, et al. Clinical Laboratory Perspective on Streptococcus halichoeri, an Unusual Nonhemolytic, Lancefield Group B Streptococcus Causing Human Infections. Emerg Infect Dis. 2021;27(5):1309-1316.  [PMID:33900169]

    Comment: Case series of patients with S. halichoeri bone and joint infections, a rare pathogen that can cause bacteremia. All isolates susceptible to beta-lactams and fluoroquinolones; vancomycin and linezolid also have excellent activity.

  5. Park C, Nichols M, Schrag SJ. Two cases of invasive vancomycin-resistant group B streptococcus infection. N Engl J Med. 2014;370(9):885-6.  [PMID:24571775]

    Comment: Letter describing two seemingly unrelated clinical cases of vancomycin resistance to GBS. Both isolates were identified as vancomycin-nonsusceptible by local and state health authorities.

  6. García-de-la-Mària C, Pericas JM, Del Río A, et al. Early in vitro and in vivo development of high-level daptomycin resistance is common in mitis group Streptococci after exposure to daptomycin. Antimicrob Agents Chemother. 2013;57(5):2319-25.  [PMID:23478959]

    Comment: This work describes experimental models demonstrating the emergence of high-level daptomycin resistance upon exposure to daptomycin among viridans Streptococci isolates initially found to be susceptible to daptomycin. The addition of low-dose gentamicin prevented the emergence of daptomycin resistance in 91% of rabbits in their model.

  7. Fairlie T, Zell ER, Schrag S. Effectiveness of intrapartum antibiotic prophylaxis for prevention of early-onset group B streptococcal disease. Obstet Gynecol. 2013;121(3):570-577.  [PMID:23635620]

    Comment: Use of at least four hours of antimicrobial prophylaxis with either penicillin or ampicillin was 86-91% effective in preventing early-onset neonatal GBS disease. Use of clindamycin was significantly less effective, highlighting the need to use cefazolin, not clindamycin, for pregnant women without a history of anaphylaxis or urticaria upon exposure to penicillins.

  8. Poncelet-Jasserand E, Forges F, Varlet MN, et al. Reduction of the use of antimicrobial drugs following the rapid detection of Streptococcus agalactiae in the vagina at delivery by real-time PCR assay. BJOG. 2013;120(9):1098-108.  [PMID:23656626]

    Comment: Molecular testing to detect genital tract GBS colonization has been extensively studied, with excellent sensitivity and specificity. This analysis found such testing to be associated with lower rates of antibiotic administration when compared with convential culture-based diagnostics at 34-38 weeks gestation. Use of molecular diagnostics may lower rates of needless antibiotic administration (and its associated sequelae) at the cost of the greater expense of real-time PCR testing.

  9. Thigpen MC, Whitney CG, Messonnier NE, et al. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011;364(21):2016-25.  [PMID:21612470]

    Comment:
    Nice epidemiologic summary of incidence rates of meningitis due to Pneumococcus, Meningococcus, L. monocytogenes, H. influenza, and S. agalactiae based upon laboratory- and population-based surveillance data. Rates of meningitis due to all pathogens, except S. agalactiae, decreased significantly over the interval.

  10. Boleij A, Muytjens CM, Bukhari SI, et al. Novel clues on the specific association of Streptococcus gallolyticus subsp gallolyticus with colorectal cancer. J Infect Dis. 2011;203(8):1101-9.  [PMID:21451000]

    Comment:
    Interesting discussion of the pathogenic mechanisms by which (a) GI tract colonization with S. gallolyticus subsp. gallolyticus might increase among persons with colorectal cancer, and (b) increased incidence rates of endocarditis caused by this pathogen among these patients might be explained.

  11. Verani JR, McGee L, Schrag SJ, et al. Prevention of perinatal group B streptococcal disease--revised guidelines from CDC, 2010. MMWR Recomm Rep. 2010;59(RR-10):1-36.  [PMID:21088663]

    Comment:
    Excellent CDC guideline statement regarding the role of screening expectant mothers and administering prophylactic antibiotic therapy to reduce rates of invasive GBS disease among newborns. The universal screening strategy initially recommended in 1996 and revised twice since then has been associated with substantial rates in reduction of early-onset invasive GBS disease.

  12. Doern CD, Burnham CA. It's not easy being green: the viridans group streptococci, with a focus on pediatric clinical manifestations. J Clin Microbiol. 2010;48(11):3829-35.  [PMID:20810781]

    Comment: A relatively easy-to-understand review of green streptococcal species, though this remains fluid with certain future changes.

  13. Wertheim HF, Nghia HD, Taylor W, et al. Streptococcus suis: an emerging human pathogen. Clin Infect Dis. 2009;48(5):617-25.  [PMID:19191650]

    Comment: Interesting review article highlighting the emergence of S. suis as a zoonotic pathogen among pig farmers, particularly in southeast Asia, where it is a not uncommon cause of meningitis and hearing loss.

  14. Sendi P, Johansson L, Norrby-Teglund A. Invasive group B Streptococcal disease in non-pregnant adults : a review with emphasis on skin and soft-tissue infections. Infection. 2008;36(2):100-11.  [PMID:18193384]

    Comment: Comprehensive review of invasive S. agalactiae infections in non-pregnant adults. The authors note that diabetes and immunocompromise increase the risk of infection. Bacteremia and skin/soft tissue infections are the most common types of infections, although toxic shock syndrome and necrotizing fasciitis are more recently recognized conditions associated with this bacterium.

  15. Nguyen TH, Tran TH, Thwaites G, et al. Dexamethasone in Vietnamese adolescents and adults with bacterial meningitis. N Engl J Med. 2007;357(24):2431-40.  [PMID:18077808]

    Comment: Although controversial, dexamethasone is now used as part of the treatment of adults with confirmed or suspected bacterial meningitis in southern Vietnam, in large part because of the positive impact on morbidity and mortality seen in cases of S. suis meningitis in this study.

  16. Edwards MS, Rench MA, Palazzi DL, et al. Group B streptococcal colonization and serotype-specific immunity in healthy elderly persons. Clin Infect Dis. 2005;40(3):352-7.  [PMID:15668856]

    Comment: Raising rates of GBS infection in the elderly may be explained by the finding that colonization rates are similar, but the elderly are more likely to be colonized by the V type that causes invasive disease.
    Rating: Important

  17. Zheng X, Freeman AF, Villafranca J, et al. Antimicrobial susceptibilities of invasive pediatric Abiotrophia and Granulicatella isolates. J Clin Microbiol. 2004;42(9):4323-6.  [PMID:15365035]

    Comment: Among 15 Abiotrophia and Granulicatella isolates, ten demonstrated intermediate resistance to penicillin, and 3 were resistant.

  18. Gold JS, Bayar S, Salem RR. Association of Streptococcus bovis bacteremia with colonic neoplasia and extracolonic malignancy. Arch Surg. 2004;139(7):760-5.  [PMID:15249410]

    Comment: Retrospective study highlights long known association with colon cancer (17/45 pts 41%), but also notes that 5/45 were found to have an extra-gastrointestinal malignancy.

  19. Facklam R. What happened to the streptococci: overview of taxonomic and nomenclature changes. Clin Microbiol Rev. 2002;15(4):613-30.  [PMID:12364372]

    Comment: Review of contemporary Streptococcus species as well as non-Streptococcal Gram-positive cocci that form chains (e.g., Abiotrophia and Granulicatella) as identified and distinguished by phenotypic and molecular technique.

  20. Claridge JE, Attorri S, Musher DM, et al. Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus ("Streptococcus milleri group") are of different clinical importance and are not equally associated with abscess. Clin Infect Dis. 2001;32(10):1511-5.  [PMID:11317256]

    Comment: The authors report data on 122 cases of Streptococcus milleri (now classified as either Streptococcus intermedius or S. anginosus Group) infection over a 1-year period. They found that 41/56 isolates of S. constellatus, 10/14 S. intermedius and 10/52 S. S. constellatus infections were associated with abscess formation. In addition, they note that S. intermedius was usually found as a monomicrobial pathogen, while S. constellatus and S. anginosus tended to cause polymicrobial infections.

  21. Pfaller MA, Jones RN, Doern GV, et al. Survey of blood stream infections attributable to gram-positive cocci: frequency of occurrence and antimicrobial susceptibility of isolates collected in 1997 in the United States, Canada, and Latin America from the SENTRY Antimicrobial Surveillance Program. SENTRY Participants Group. Diagn Microbiol Infect Dis. 1999;33(4):283-97.  [PMID:10212756]

    Comment: Penicillin resistance among viridans group streptococci shown to have reached 48.5% in U.S among isolates tested.
    Rating: Important

  22. Schattner A, Vosti KL. Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore). 1998;77(2):122-39.  [PMID:9556703]

    Comment: Group A, B and G account for most cases, with only Group A associated with toxic-shock-like features.
    Rating: Important

  23. Colford JM, Mohle-Boetani J, Vosti KL. Group B streptococcal bacteremia in adults. Five years' experience and a review of the literature. Medicine (Baltimore). 1995;74(4):176-90.  [PMID:7623653]

    Comment: This report is similar to five earlier studies, which show that GBS in adult patients is most common in those over 50 years old (66%). Primary bacteremia was the most frequent clinical diagnosis, occurring in 7 (22%) of 32 patients. Nonhematologic cancer was the most frequently associated condition (25%). Nineteen percent of the patients had diabetes mellitus. The overall mortality rate was 31% and was significantly associated with increasing age.

  24. Shinzato T, Saito A. The Streptococcus milleri group as a cause of pulmonary infections. Clin Infect Dis. 1995;21 Suppl 3:S238-43.  [PMID:8749672]

    Comment: A study utilizing percutaneous microbiologic specimens of pulmonary infiltrates and pleural collections. A high proportion were found to involve organisms of the Streptococcus milleri group, and synergy provided by oral anaerobic bacteria was demonstrated too.

  25. Elting LS, Bodey GP, Keefe BH. Septicemia and shock syndrome due to viridans streptococci: a case-control study of predisposing factors. Clin Infect Dis. 1992;14(6):1201-7.  [PMID:1623076]

    Comment: Report highlights the growing emergence of severe bacteremia (often continuous) in patients undergoing chemotherapy. Between 1972 and 1989, the incidence of viridans streptococcal bacteremia at the University of Texas M. D. Anderson Cancer Center in Houston increased from one case per 10,000 admissions to 47 cases per 10,000 admissions (P less than .0001). Risk factors also included TMP-SMX or FQ use, use of antacids leading others to suspect gastric source from chemotherapy-induced irritation. A shock syndrome w/hypotension, rash, palmar desquamation, ARDS developed in 26% of patients.
    Rating: Important

  26. Swenson FJ, Rubin SJ. Clinical significance of viridans streptococci isolated from blood cultures. J Clin Microbiol. 1982;15(4):725-7.  [PMID:7068840]

    Comment: Frequently cited paper indicating a high rate of rejection of blood cultures growing viridans streptococci as being contaminants (approximately 4 of 5 were felt to be such). This paper again highlights the "art" of medicine in the need to carefully weigh each situation rather than to have "knee jerk" responses to clinical microbiological data.
    Rating: Important

Media

α, β and γ hemolysis in Streptococcus species

Descriptive text is not available for this image

Isolates: (left) α-hemolysis (S. mitis); (middle) β-hemolysis (S. pyogenes); (right) γ-hemolysis (= non-hemolytic, S. salivarius)

Source: Y tambe, Wikimedia commons

Last updated: November 20, 2025