Invasive GAS: Necrotizing Fasciitis and Streptococcal Toxic Shock

What Makes GAS Invasive

A 2014 review describes a large number of GAS virulence factors, many overlapping in function, that help the bacteria attach to and colonize tissue, resist the innate immune system, and break down tissue barriers to spread within the body (PubMed PMID: 24696436).

The best-known surface protein is the M protein, described in a 1989 review as a major virulence factor because it allows the organism to resist phagocytosis, the immune system’s engulfing of bacteria (PubMed PMID: 2670192). Strains are typed by their M protein gene (emm type). In European surveillance of 5,521 severe cases in 2003–2004, 104 emm types were found; STSS and necrotizing fasciitis were caused by many types but were particularly associated with emm1 and emm3 (PubMed PMID: 19158266). In US surveillance, emm type 1 or 3 was one of the factors independently associated with death (PubMed PMID: 27105747).

GAS also makes streptococcal pyrogenic exotoxins, which act as superantigens (PubMed PMID: 28779832). A 2002 review counts 19 different superantigens produced by S. aureus and S. pyogenes together (PubMed PMID: 11944185). In a 1989 report of 20 patients with severe GAS infection and a toxic shock-like syndrome in the Rocky Mountain region, 8 of 10 tested strains produced pyrogenic exotoxin A (scarlet fever toxin A), which the authors noted had rarely been observed in recent years; most of the patients had no underlying disease (PubMed PMID: 2659990).

The CDC states that the bacteria that cause necrotizing fasciitis most commonly enter through a break in the skin, such as burns, cuts and scrapes, insect bites, puncture wounds and surgical wounds, and that the infection can also follow blunt trauma (CDC: About necrotizing fasciitis).

A 2005 global estimate put the burden of invasive GAS disease at at least 663,000 new cases and 163,000 deaths each year, within at least 517,000 deaths a year from all severe GAS diseases; the authors noted that data from developing countries are poor (PubMed PMID: 16253886). In the United States, surveillance in 2005–2012 found 3.8 cases per 100,000 people per year and an overall case-fatality rate of 11.7% (PubMed PMID: 27105747). The 2014 review notes that GAS remains sensitive to all penicillins and cephalosporins (PubMed PMID: 24696436).

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Necrotizing Fasciitis Type II

Necrotizing fasciitis (NF) is an infection of the fascia, the connective tissue around muscles. A 2017 review classes necrotizing soft-tissue infections into Type I, polymicrobial, an estimated 70–80% of cases, and Type II, often monomicrobial and usually caused by GAS or occasionally Staphylococcus aureus, an estimated 20–30% (PubMed PMID: 28779832). In a Dutch series of 58 intensive-care patients, 23 (39.7%) had Type 2 infection and mortality was 29.3% (PubMed PMID: 27239222). The same 2017 review describes Fournier’s gangrene, necrotizing infection of the perineum, as generally polymicrobial (PubMed PMID: 28779832).

Mortality figures, by source:

• The CDC’s clinical guidance states that in the most recent 5 years the mortality of streptococcal necrotizing fasciitis has been around 15 to 20% (CDC: Clinical guidance for necrotizing fasciitis), and its patient page states that even with treatment up to 1 in 5 people died from the infection (CDC: About necrotizing fasciitis).
• In US surveillance of invasive GAS in 2005–2012, the case-fatality rate for NF was 29% when it was the only syndrome present (PubMed PMID: 27105747).
• Across all types of necrotizing soft-tissue infection, a 2020 systematic review of 109 studies (6,051 patients) found that 1,277 patients died (21.1%), with average reported mortality staying around 20% over the past 20 years (PubMed PMID: 31921330).

Timing of surgery has been studied directly. The 2020 meta-analysis found lower mortality with surgery within 6 hours of presentation than with later surgery (19% vs 32%; OR 0.43, 95% CI 0.26–0.70; 10 studies) and with surgery within 12 hours (OR 0.41, 95% CI 0.27–0.61; 16 studies); patient delay before presentation did not significantly affect mortality, and none of the time-related variables significantly reduced the amputation rate (PubMed PMID: 31921330).

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Clinical Warning Signs of NF

The CDC’s clinical guidance describes Type II necrotizing fasciitis as follows (CDC: Clinical guidance for necrotizing fasciitis):

1. Early: it usually begins with pain in the affected area accompanied by redness, heat, swelling and tenderness, and the pain is usually out of proportion to the signs of the local skin infection.
2. Within 24 to 48 hours: the overlying skin may turn dusky, the skin becomes ischemic, and blisters (bullae) form and fill with straw-colored fluid.
3. Later: the bullae turn dark with hemorrhagic fluid, and affected tissues progressively darken from red to purple to blue to black.

The CDC’s patient page lists early symptoms as a red, warm or swollen area of skin that spreads quickly, fever, and severe pain, including beyond the area that is red, warm or swollen; later symptoms include changes in skin color, diarrhea or nausea, dizziness, fatigue, pus or oozing, and ulcers, blisters or black spots on the skin (CDC: About necrotizing fasciitis). The 2017 review notes that it can often be difficult to tell a necrotizing process from a simple cellulitis (PubMed PMID: 28779832).

A 2019 meta-analysis of 23 studies (5,982 patients) pooled the accuracy of single findings: fever had a sensitivity of 46.0%, hemorrhagic bullae 25.2% and hypotension 21.0%, and the authors concluded that the absence of any one physical-examination feature is not sufficient to rule out a necrotizing soft-tissue infection. Computed tomography (CT) had a sensitivity of 88.5% and specificity of 93.3%, against 48.9% and 94.0% for plain radiography, and given the poor sensitivity of the tests the authors concluded that high clinical suspicion warrants early surgical consultation (PubMed PMID: 29672405). The CDC’s clinical guidance states that imaging may be helpful but should never delay surgical exploration (CDC: Clinical guidance for necrotizing fasciitis).

At operation, the 2017 review describes the fascia being examined for necrosis, “dishwater” brown fluid, or a positive “finger sign”, in which a finger inserted along the fascial planes easily dissects the overlying tissue without resistance (PubMed PMID: 28779832).

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Streptococcal Toxic Shock Syndrome

The 2017 review describes the mechanism: pyrogenic exotoxins act as superantigens that bind to antigen-presenting cells and cause rapid proliferation of T cells, and the resulting cytokine production drives shock and multi-organ failure. It reports toxic shock syndrome in up to half of necrotizing soft-tissue infections due to GAS (PubMed PMID: 28779832). A 2002 review describes superantigens as protein exotoxins that trigger excessive and aberrant activation of T cells (PubMed PMID: 11944185).

A consensus definition was published by the Working Group on Severe Streptococcal Infections in 1993 (PubMed PMID: 8418347). The CDC’s 2010 surveillance case definition requires isolation of GAS, hypotension (systolic blood pressure of 90 mm Hg or less in adults, or below the fifth percentile for age in children under 16) and two or more of: kidney impairment, coagulopathy (low platelets or disseminated intravascular coagulation), liver involvement, acute respiratory distress syndrome, a generalized red macular rash that may peel, or soft-tissue necrosis including necrotizing fasciitis, myositis or gangrene (CDC: STSS 2010 case definition).

The CDC lists first symptoms of STSS as fever and chills, muscle aches, and nausea and vomiting, followed by low blood pressure, organ failure, a fast heart rate and rapid breathing (CDC: About STSS).

Mortality figures, by source:

• The CDC’s clinical guidance states that despite aggressive treatment the mortality rate for STSS can exceed 30%, that it increases with age, and that it is substantially lower in children than in adults (CDC: Clinical guidance for STSS).
• In US surveillance in 2005–2012, the case-fatality rate was 38% for STSS and 45% for septic shock when each was the only syndrome present; 70% of patients aged 65 or older with STSS alone died (PubMed PMID: 27105747).
• In Ontario surveillance of children in 1992–1996, the case-fatality rate was 56% for STSS, 10% for NF and 4% overall (PubMed PMID: 10799624).

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Bacteremia and Other Invasive Forms

US surveillance of 9,557 invasive GAS cases in 2005–2012 gives the range of forms the infection takes and how often each was fatal (PubMed PMID: 27105747):

• Skin and soft-tissue infection was the most common presentation (41% of patients).
• Isolated bacteremia (GAS in the blood with no clinical syndrome identified) made up 25% of cases, with a case-fatality rate of 14.3%, and was one of the syndromes independently associated with death.
• Pneumonia made up 16% of cases (case-fatality 18.8%) and was more common in patients aged 65 or older.
• Meningitis or other central nervous system infection was uncommon (1.2%) but had a case-fatality rate of 23.6%.
• Septic arthritis (10.3%) and osteomyelitis (4.5%) were more common in children under 10, as were meningitis and isolated bacteremia.
• Endocarditis or pericarditis made up 1.4% of cases.

Those with septic shock, STSS, NF, meningitis or pneumonia had the highest case-fatality rates in that surveillance (PubMed PMID: 27105747).

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Postpartum Sepsis

In the Vienna maternity clinics of the 1840s, Ignaz Semmelweis observed that maternal mortality was far higher in the clinic where medical students worked than in the clinic staffed by midwives. After a colleague died of sepsis in 1847 following a cut during an autopsy, he attributed the deaths to “cadaverous particles” carried on hands and had staff wash their hands in a chlorinated lime solution, after which mortality in the first clinic fell sharply, according to a 2024 historical review (PubMed PMID: 39553012).

A 2013 review of published cases from 1974 to 2009 states that puerperal sepsis caused by GAS remains an important cause of maternal and infant death worldwide, including in countries with modern antibiotics, intensive care and infection control, and that the pathogenesis of pregnancy-related GAS infection in modern times is complex and not simply the result of exposure to GAS in hospital (PubMed PMID: 23645851). In US surveillance in 2005–2012, pregnancy-related infections in women aged 15–44 included endometritis, septic abortion, chorioamnionitis and puerperal sepsis, with a case-fatality rate of 2.5% (PubMed PMID: 27105747).

The CDC’s clinical guidance names penicillin and clindamycin used together as the first-line antibiotics for STSS, with removal of the source of infection where possible (CDC: Clinical guidance for STSS).

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Risk Factors for Invasive GAS

The CDC lists the following as raising the risk of serious GAS infection (CDC: About group A strep):

• Viral infections, such as flu or chickenpox
• Cancer; chronic heart, kidney, liver or lung disease; diabetes; a weakened immune system; obesity; and wounds or skin disease
• Age 65 or older; injecting drugs or experiencing homelessness; living in a long-term care facility; and American Indian, Alaska Native, Native Hawaiian and Pacific Islander populations

For STSS specifically, the CDC’s clinical guidance lists age 65 or older, alcohol use disorder, diabetes, recent surgery, a viral infection that causes open sores (such as varicella) or other skin injury, and states that NSAID use may increase risk (CDC: Clinical guidance for STSS).

Chickenpox. In Ontario surveillance of children, 15% of children with invasive GAS had preceding chickenpox, which significantly increased the risk of invasive GAS disease (RR 58), and children with recent chickenpox were more likely to have NF (RR 6.3) (PubMed PMID: 10799624).

NSAIDs (debated). In a French pharmacovigilance case-control study of 38 necrotizing soft-tissue infections (mostly children; 25 exposed to ibuprofen, 24 with chickenpox), the adjusted odds ratio for NSAID exposure was 31.38 (95% CI 6.40–153.84); the authors noted the limits of a spontaneous-reporting system, could not conclude whether NSAIDs raise the risk in all patients, and suggested they may mask symptoms and delay diagnosis (PubMed PMID: 18261144). The CDC’s necrotizing fasciitis guidance states that retrospective reports linked NSAIDs to necrotizing fasciitis but prospective studies have not confirmed the link (CDC: Clinical guidance for necrotizing fasciitis). In STSS, a 2022 meta-analysis was uncertain whether NSAIDs increase the odds of death (OR 4.14, 50 patients, very low certainty) (PubMed PMID: 36456018).

Factors linked to death. In US surveillance, increasing age, nursing-home residence, recent surgery, septic shock, NF, meningitis, isolated bacteremia, pneumonia, emm type 1 or 3, and underlying chronic illness or immunosuppression were independently associated with death (PubMed PMID: 27105747). In STSS, the 2022 meta-analysis found that the odds of death may be higher at age 65 or older than at 18–64 (OR 2.37, low certainty) (PubMed PMID: 36456018).

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Treatment: Antibiotics, Surgery and IVIG

The CDC’s clinical guidance describes early and aggressive surgical exploration with debridement of necrotic tissue as the primary treatment of necrotizing fasciitis, and high-dose penicillin and clindamycin once GAS is confirmed (CDC: Clinical guidance for necrotizing fasciitis). For STSS it names penicillin and clindamycin together as first-line antibiotics and notes that surgical debridement of deep tissue infection may be necessary (CDC: Clinical guidance for STSS).

Why Clindamycin Is Added to Penicillin

Harry Eagle’s 1952 experiments examined penicillin treatment failure in mice with GAS infection (PubMed PMID: 12985596). In a 1988 mouse model of streptococcal myositis, penicillin was ineffective unless given at the time of bacterial injection, while clindamycin-treated mice had survival rates of 100%, 100%, 80% and 70% when treatment was delayed 0, 2, 6 and 16.5 hours; the authors suggested that, unlike penicillin, clindamycin is not affected by the “Eagle effect” (PubMed PMID: 3292661). These are animal results.

The 2017 review describes clindamycin as working by inhibiting the bacterial ribosome, with an effect independent of inoculum size or stage of infection and potential antitoxin properties; in toxic shock it is thought to lessen shock by decreasing toxin production. The review states that the Surgical Infection Society and IDSA guidelines both strongly recommend penicillin plus clindamycin in necrotizing soft-tissue infection due to GAS (PubMed PMID: 28779832). The human evidence is observational:

• In 1,079 patients with invasive GAS treated with beta-lactams in US hospitals, in-hospital mortality among propensity-matched patients was 6.5% with adjunctive clindamycin and 11.0% without (adjusted OR 0.44, 95% CI 0.23–0.81); the authors began by noting that there had been little evidence of a benefit in humans (PubMed PMID: 33333013).
• In 257 patients hospitalized for invasive GAS in Florida, clindamycin was associated with lower mortality in those with necrotizing fasciitis (OR 0.11, 95% CI 0.01–0.89) but not in those without it (OR 1.01) (PubMed PMID: 14570340).
• In 67 Swedish patients with STSS, clindamycin (OR 8.6) and IVIG (OR 5.6) were each associated with survival in adjusted analysis (PubMed PMID: 24928291).
• A 2022 meta-analysis in STSS found clindamycin treatment associated with lower mortality (OR 0.14, 95% CI 0.06–0.37), with low certainty of evidence (PubMed PMID: 36456018).

IVIG for Toxic Shock

Intravenous immunoglobulin (IVIG) is proposed to bind and inactivate circulating superantigens, blunting the cytokine cascade (PubMed PMID: 28779832). The CDC states that IVIG can be considered for severely ill STSS patients early in the course, although efficacy has not been proven (CDC: Clinical guidance for STSS). The studies, in order:

• Kaul et al. (1999): 21 consecutive STSS patients given IVIG were compared with 32 earlier patients who did not receive it; 30-day survival was 67% versus 34% (odds ratio for survival 8.1, 95% CI 1.6–45). This was an observational comparison, not a randomized trial (PubMed PMID: 10825042).
• Darenberg et al. (2003): a European randomized, double-blind, placebo-controlled trial in STSS was stopped early because of slow recruitment, with 21 patients enrolled. Mortality at 28 days was 3.6-fold higher in the placebo group, but the primary end point did not reach statistical significance (PubMed PMID: 12884156).
• Linnér et al. (2014): in the 67 Swedish STSS patients above, IVIG was associated with survival (OR 5.6); the IVIG group had more necrotizing fasciitis (56% vs 14%) and the study was observational (PubMed PMID: 24928291).
• INSTINCT (2017): a randomized, blinded, placebo-controlled trial in 100 intensive-care patients with necrotizing soft-tissue infection, given 25 g of IVIG or saline daily for 3 days, found no apparent effect on self-reported physical function at 6 months (median score 36 vs 31; p = 0.81) (PubMed PMID: 28421246).
• Kadri et al. (2017): among 4,127 patients with debrided necrotizing fasciitis and vasopressor-dependent shock at US hospitals, 164 (4%) received IVIG; in-hospital mortality did not differ between matched groups (27.3% vs 23.6%; adjusted OR 1.00), and among patients coded for toxic shock, GAS or S. aureus IVIG also showed no benefit (PubMed PMID: 28034881).
• Meta-analyses in clindamycin-treated STSS: one found mortality fell from 33.7% to 15.7% in association with IVIG across one randomized and four nonrandomized studies (PubMed PMID: 29788397); another found an association between IVIG and lower mortality (OR 0.34, 95% CI 0.15–0.75), with low certainty of evidence (PubMed PMID: 36456018).

The STSS studies report lower mortality with IVIG, mostly from nonrandomized data, while the INSTINCT trial and the US cohort, both in broader necrotizing-infection populations, found no benefit. The 2017 review concludes that adjuvant IVIG is not likely to improve survival or quality of life and is best reserved for case-by-case use (PubMed PMID: 28779832).

Surgical Debridement

The 2017 review states that delay in identification or early surgical management clearly increases mortality, that in survivors delay also increases the number of later operations needed, and that wounds are typically re-explored in the operating room within 24–48 hours of the first debridement (PubMed PMID: 28779832). The time-to-surgery figures from the 2020 meta-analysis are given in the Necrotizing Fasciitis section above (PubMed PMID: 31921330).

When Health Agencies Say to Seek Care

The CDC’s patient page advises seeing a healthcare provider right away for the symptoms of necrotizing fasciitis listed above, particularly after an injury or surgery (CDC: About necrotizing fasciitis), and advises seeking medical attention immediately for symptoms of STSS (CDC: About STSS). Decisions about diagnosis and treatment belong with a clinician.

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Key Research Papers

1. Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med. 2017;377(23):2253-2265. — PubMed PMID: 29211672
2. The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome: rationale and consensus definition. JAMA. 1993;269(3):390-391. — PubMed PMID: 8418347
3. Walker MJ, Barnett TC, McArthur JD, et al. Disease manifestations and pathogenic mechanisms of Group A Streptococcus. Clin Microbiol Rev. 2014;27(2):264-301. — PubMed PMID: 24696436
4. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005;5(11):685-694. — PubMed PMID: 16253886
5. Carapetis JR, McDonald M, Wilson NJ. Acute rheumatic fever. Lancet. 2005;366(9480):155-168. — PubMed PMID: 16005340
6. van Stigt SF, de Vries J, Bijker JB, et al. Review of 58 patients with necrotizing fasciitis in the Netherlands. World J Emerg Surg. 2016;11:21. — PubMed PMID: 27239222
7. Linnér A, Darenberg J, Sjölin J, Henriques-Normark B, Norrby-Teglund A. Clinical efficacy of polyspecific intravenous immunoglobulin therapy in patients with streptococcal toxic shock syndrome: a comparative observational study. Clin Infect Dis. 2014;59(6):851-857. — PubMed PMID: 24928291
8. Hamilton SM, Stevens DL, Bryant AE. Pregnancy-related group a streptococcal infections: temporal relationships between bacterial acquisition, infection onset, clinical findings, and outcome. Clin Infect Dis. 2013;57(6):870-876. — PubMed PMID: 23645851
9. Luca-Harari B, Darenberg J, Neal S, et al. Clinical and microbiological characteristics of severe Streptococcus pyogenes disease in Europe. J Clin Microbiol. 2009;47(4):1155-1165. — PubMed PMID: 19158266
10. Mulla ZD, Leaverton PE, Wiersma ST. Invasive group A streptococcal infections in Florida. South Med J. 2003;96(10):968-973. — PubMed PMID: 14570340
11. Nelson GE, Pondo T, Toews KA, et al. Epidemiology of invasive group A streptococcal infections in the United States, 2005-2012. Clin Infect Dis. 2016;63(4):478-486. — PubMed PMID: 27105747
12. Bonne SL, Kadri SS. Evaluation and management of necrotizing soft tissue infections. Infect Dis Clin North Am. 2017;31(3):497-511. — PubMed PMID: 28779832
13. Fischetti VA. Streptococcal M protein: molecular design and biological behavior. Clin Microbiol Rev. 1989;2(3):285-314. — PubMed PMID: 2670192
14. Stevens DL, Tanner MH, Winship J, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med. 1989;321(1):1-7. — PubMed PMID: 2659990
15. Llewelyn M, Cohen J. Superantigens: microbial agents that corrupt immunity. Lancet Infect Dis. 2002;2(3):156-162. — PubMed PMID: 11944185
16. Nawijn F, Smeeing DPJ, Houwert RM, Leenen LPH, Hietbrink F. Time is of the essence when treating necrotizing soft tissue infections: a systematic review and meta-analysis. World J Emerg Surg. 2020;15:4. — PubMed PMID: 31921330
17. Fernando SM, Tran A, Cheng W, et al. Necrotizing soft tissue infection: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-analysis. Ann Surg. 2019;269(1):58-65. — PubMed PMID: 29672405
18. Laupland KB, Davies HD, Low DE, et al. Invasive group A streptococcal disease in children and association with varicella-zoster virus infection. Pediatrics. 2000;105(5):E60. — PubMed PMID: 10799624
19. Souyri C, Olivier P, Grolleau S, Lapeyre-Mestre M. Severe necrotizing soft-tissue infections and nonsteroidal anti-inflammatory drugs. Clin Exp Dermatol. 2008;33(3):249-255. — PubMed PMID: 18261144
20. Bartoszko JJ, Elias Z, Rudziak P, et al. Prognostic factors for streptococcal toxic shock syndrome: systematic review and meta-analysis. BMJ Open. 2022;12(12):e063023. — PubMed PMID: 36456018
21. Eagle H. Experimental approach to the problem of treatment failure with penicillin. I. Group A streptococcal infection in mice. Am J Med. 1952;13(4):389-399. — PubMed PMID: 12985596
22. Stevens DL, Gibbons AE, Bergstrom R, Winn V. The Eagle effect revisited: efficacy of clindamycin, erythromycin, and penicillin in the treatment of streptococcal myositis. J Infect Dis. 1988;158(1):23-28. — PubMed PMID: 3292661
23. Babiker A, Li X, Lai YL, et al. Effectiveness of adjunctive clindamycin in β-lactam antibiotic-treated patients with invasive β-haemolytic streptococcal infections in US hospitals: a retrospective multicentre cohort study. Lancet Infect Dis. 2021;21(5):697-710. — PubMed PMID: 33333013
24. Kaul R, McGeer A, Norrby-Teglund A, et al. Intravenous immunoglobulin therapy for streptococcal toxic shock syndrome — a comparative observational study. Clin Infect Dis. 1999;28(4):800-807. — PubMed PMID: 10825042
25. Darenberg J, Ihendyane N, Sjölin J, et al. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial. Clin Infect Dis. 2003;37(3):333-340. — PubMed PMID: 12884156
26. Madsen MB, Hjortrup PB, Hansen MB, et al. Immunoglobulin G for patients with necrotising soft tissue infection (INSTINCT): a randomised, blinded, placebo-controlled trial. Intensive Care Med. 2017;43(11):1585-1593. — PubMed PMID: 28421246
27. Kadri SS, Swihart BJ, Bonne SL, et al. Impact of intravenous immunoglobulin on survival in necrotizing fasciitis with vasopressor-dependent shock: a propensity score-matched analysis from 130 US hospitals. Clin Infect Dis. 2017;64(7):877-885. — PubMed PMID: 28034881
28. Parks T, Wilson C, Curtis N, Norrby-Teglund A, Sriskandan S. Polyspecific intravenous immunoglobulin in clindamycin-treated patients with streptococcal toxic shock syndrome: a systematic review and meta-analysis. Clin Infect Dis. 2018;67(9):1434-1436. — PubMed PMID: 29788397
29. Paul S, Salunkhe S, Sravanthi K, Mane SV. Pioneering hand hygiene: Ignaz Semmelweis and the fight against puerperal fever. Cureus. 2024;16(10):e71689. — PubMed PMID: 39553012

PubMed Topic Searches

1. PubMed: Necrotizing fasciitis Streptococcus treatment
2. PubMed: Streptococcal toxic shock syndrome superantigen
3. PubMed: Invasive group A streptococcus bacteremia outcomes
4. PubMed: Clindamycin penicillin invasive streptococcal infection
5. PubMed: Postpartum group A streptococcal sepsis

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Connections

• All Bacteria
• Streptococcus Pyogenes Overview
• Strep Symptoms & Diagnosis
• Penicillin & Antibiotic Treatment
• Strep Treatment & Prevention
• Infectious Disease
• Necrotizing Fasciitis — the full disease page, covering Type I polymicrobial cases as well as the Type II strep infection described here.
• Prevention & Vaccines
• Complications

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