Intravenous Immunoglobulin as Adjunctive Treatment for Streptococcal Toxic Shock Syndrome Associated with Necrotizing Fasciitis: Case Report and Review

Cawley, Michael J.; Briggs, Michael H.; Haith, Linwood R.; Reilly, Kathleen J.; Guilday, Robert E.; Braxton, Gayna R.; Patton, Mary Lou

doi:10.1592/phco.19.13.1094.31589

Cited by 76 publications

(29 citation statements)

References 28 publications

(26 reference statements)

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“…Case-control studies show a reduction of mortality from 67 to 34% 36 . Although a randomized clinical trial has never been conducted, most experts advocate the use of IVIG -preferably early in the disease course -for patients with shock due to invasive GAS infections [37][38][39] . This case represents the first report utilizing IVIG in GAS TSS occurring in the puerperium and reminds clinicians to include invasive GAS in the differential diagnosis of a puerperal infection when a patient presents with the rapid onset of septic shock.…”

Section: First Author/ Referencementioning

confidence: 99%

Group A Streptococcal Toxic Shock Syndrome Developing inthe Third Trimester of Pregnancy

Crum

Chun

Gaylord

et al. 2002

Infectious Diseases in Obstetrics and Gynecology

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Background: Group A streptococcal (GAS) toxic shock syndrome (TSS) is an uncommon, but life-threatening infection during pregnancy and should be considered in rapid onset of shock. Most cases described in the literature have occurred in the puerperium. We report a case of GAS TSS occurring during the third trimester of pregnancy in a previously healthy woman. Case: A 31-year-old female, who was 34 weeks pregnant, presented with fevers and a prodromal 'flu-like' illness. She rapidly developed shock and multiorgan failure. Blood cultures revealed GAS bacteremia and the patient met criteria for streptococcal TSS. Despite her eventual recovery, her infant died on postpartum day 15 as a consequence of the mother's TSS. Conclusions: This case is unusual in that there were no identifiable initiating events or source of the streptococcal infection, and the TSS developed during pregnancy rather than after delivery. Early recognition of GAS infections is important given the rapid onset and high morbidity and mortality associated with these infections. This is the first reported case utilizing intravenous immunoglobulin for GAS TSS in the puerperium.

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Section: First Author/ Referencementioning

confidence: 99%

Group A Streptococcal Toxic Shock Syndrome Developing inthe Third Trimester of Pregnancy

Crum

Chun

Gaylord

et al. 2002

Infectious Diseases in Obstetrics and Gynecology

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“…It would be interesting to test whether these MAbs have therapeutic value against severe invasive infections. In addition, intravenous immunoglobulin treatment is actually an adjunctive treatment for severe invasive infections (6). Developing MAbs effective for enhancing GAS killing by the innate immune system may eventually lead to an efficacious immunotherapy for treating severe invasive GAS infections.…”

Section: Discussionmentioning

confidence: 99%

“…Prompt surgical debridement, fluid and electrolyte management, and analgesia are mainstays of therapy for necrotizing fasciitis (5-7). Clindamycin, hyperbaric oxygen therapy, and intravenous immunoglobulin are used as adjunctive treatments of severe invasive GAS infections (4)(5)(6)(7). New strategies to treat severe GAS infections are desirable.…”

mentioning

confidence: 99%

A Neutralizing Monoclonal IgG1 Antibody of Platelet-Activating Factor Acetylhydrolase SsE Protects Mice against Lethal Subcutaneous Group A Streptococcus Infection

et al. 2015

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Group A Streptococcus (GAS) can cause life-threatening invasive infections, including necrotizing fasciitis. There are no effective treatments for severe invasive GAS infections. The platelet-activating factor (PAF) acetylhydrolase SsE produced by GAS is required for invasive GAS to evade innate immune responses and to invade soft tissues. This study determined whether the enzymatic activity of SsE is critical for its function in GAS skin invasion and inhibition of neutrophil recruitment and whether SsE is a viable target for immunotherapy for severe invasive GAS infections. An isogenic derivative of M1T1 strain MGAS5005 producing SsE with an S178A substitution (SsE S178A ), an enzymatically inactive SsE mutant protein, was generated. This strain induced higher levels of neutrophil infiltration and caused smaller lesions than MGAS5005 in subcutaneous infections of mice. This phenotype is similar to that of MGAS5005 sse deletion mutants, indicating that the enzymatic activity of SsE is critical for its function. An anti-SsE IgG1 monoclonal antibody (MAb), 2B11, neutralized the PAF acetylhydrolase activity of SsE. Passive immunization with 2B11 increased neutrophil infiltration, reduced skin invasion, and protected mice against MGAS5005 infection. However, 2B11 did not protect mice when it was administered after MGAS5005 inoculation. MGAS5005 induced vascular effusion at infection sites at early hours after GAS inoculation, suggesting that 2B11 did not always have access to infection sites. Thus, the enzymatic activity of SsE mediates its function, and SsE has the potential to be included in a vaccine but is not a therapeutic target. An effective MAb-based immunotherapy for severe invasive GAS infections may need to target virulence factors that are critical for systemic survival of GAS. G roup A Streptococcus (GAS) is a major human pathogen that commonly causes pharyngitis and superficial skin infections (1). This pathogen can also cause severe invasive infections, such as necrotizing fasciitis, streptococcal toxic shock syndrome, pneumonia, and bacteremia. Streptococcal necrotizing fasciitis results from GAS infection of the subcutaneous tissue, which progresses rapidly, causes necrosis of the fascia and subcutaneous tissue, and leads to systemic infection (2). Annually in the United States, there are more than 10 million cases of streptococcal pharyngitis and about 10,000 cases of invasive GAS infections (3.5 cases per 100,000 persons), with a fatality rate of 13.7%, and invasive infections are most frequently caused by serotype M1, M3, and M12 GAS strains (3).While antibiotic treatment is effective to treat pharyngitis patients, it is not effective for treating severe invasive GAS infections (4). Prompt surgical debridement, fluid and electrolyte management, and analgesia are mainstays of therapy for necrotizing fasciitis (5-7). Clindamycin, hyperbaric oxygen therapy, and intravenous immunoglobulin are used as adjunctive treatments of severe invasive GAS infections (4-7). New strategies to treat severe GAS inf...

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“…Several case reports have demonstrated clinical improvement after IVIG therapy of patients with severe invasive GAS infections including STSS, NF, and necrotizing myositis (Barry et al, 1992;Cawley et al, 1999;Chiu et al, 1997;Lamothe et al, 1995;Mahieu et al, 1995;Nadal et al, 1993;Perez et al, 1997;Stegmayr et al, 1992;Yong, 1994).…”

Section: Novel Therapeutic Strategiesmentioning

confidence: 99%

Severe Invasive Group a Streptococcal Infections

Norrby‐Teglund¹,

McGeer²,

Kotb³

et al. 2004

Reemergence of Established Pathogens in the 21st Century

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Intravenous Immunoglobulin as Adjunctive Treatment for Streptococcal Toxic Shock Syndrome Associated with Necrotizing Fasciitis: Case Report and Review

Cited by 76 publications

References 28 publications

Group A Streptococcal Toxic Shock Syndrome Developing inthe Third Trimester of Pregnancy

Group A Streptococcal Toxic Shock Syndrome Developing inthe Third Trimester of Pregnancy

A Neutralizing Monoclonal IgG1 Antibody of Platelet-Activating Factor Acetylhydrolase SsE Protects Mice against Lethal Subcutaneous Group A Streptococcus Infection

Severe Invasive Group a Streptococcal Infections

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